Neurology 1

Much of the information gathered is taken from Dr. Norbert Kovács’ document titled “Neurological physical examination” found here.

“A” Neurological physical examination

Example of a negative status

Skull and spinal cord are intact, with no sign of injury. Neck movements are free, there are no meningeal signs. Accurate vision, the visual field is full. Isocoria, mid-dilated pupils, maintained light reactions. Eye movements are free, with no double vision, no nystagmus. No trigeminal or facial nerve dysfunction. Symmetrical palatal arches, palatal and pharyngeal reflexes, no uvula deviation. The tongue is in the midline, its movements are free. The muscle tone is normal. Muscle trophy is normal. There is no paresis. Mid-brisk, symmetrical deep tendon reflexes. There are no pyramidal signs or pathological reflexes. No sensory loss. Coordination is precise. Normal posture, gait, and speech. Alert and oriented.

1. Examination of the skull, spine, and meningeal signs

  • Skull
    • Skull intact?
    • Bruises or bumps?
  • Spine
    • Spine straight? Lordosis/kyphosis/scoliosis?
    • No bruises
    • Paraspinal muscles have normal tone?
    • Spinal movements normal?
  • Meningeal signs
    • Not examined in people with suspected cervical spinal injury!
      • May cause myelopathy
    • These tests are based on the fact that in meningitis, stretching the meninges are painful
      • These examinations stretch the meninges, causing pain and reflex movements which reduce the stretch of the meninges
    • Positive in:
      • Meningitis
      • Subarachnoid haemorrhage
      • Meningism
        • = presence of meningeal signs in systemic diseases without CNS involvement
    • Nuchal rigidity
      • Procedure
        • Patient lies supine
        • Passively lift patient’s head
      • Negative:
        • No resistance when lifting head
        • Pain may or may not be present
      • Positive:
        • Resistance when lifting head
        • Placing chin on chest is impossible
    • Kernig sign
      • Method 1
        • Procedure
          • Patient lies supine and bends their hips and knees to 90 degrees
          • Extend one leg passively while keeping the hip flexed
          • Repeat for other leg
        • Negative:
          • No pain or resistance when extending leg
        • Positive:
          • Pain or resistance when extending leg on both sides
      • Method 2 (similar to Lasègue)
        • Procedure
          • Patient lies supine with legs straight
          • Passively raise one leg while keeping knee straight
          • Repeat for other leg
        • Negative:
          • No pain, and patient doesn’t bend the knee on their own
        • Positive:
          • Pain, and patient bends the knee on their own
    • Brudzinski sign
      • Procedure
        • Patient lies supine with legs straight
        • Passively bend patient’s head forward
      • Negative
        • No flexion on the knees or hip
      • Positive
        • Patient flexes knees and hip

2. Examination of first and second cranial nerves (smell sensation, vision)

  • CN I – olfactory nerve
    • Only tested if patient has complaints regarding smell (rare)
    • Procedure
      • Close patient’s eyes and one nostril
      • Let patient smell a non-irritating fragrance
    • Negative:
      • Patient can recognize that there is a smell (primary perception normal)
      • Patient can recognize the smell (cognitive function normal)
  • CN II – optic nerve
    • Examination of visual acuity
      • Stand 5 meters from the patient
      • Hold up a number of fingers with your hand and ask the patient to say the number
      • If patient can’t see: repeat at 4 meter distance, and so on
      • Document: “patient can count fingers at X meter distance”
    • Examination of fundus
      • With ophthalmoscopy
    • Examination of visual field
      • Stand an arm’s length away from patient
      • Have your finger outside the visual field and move it slowly towards the visual field
      • Instruct patient to tell you when they see your finger
      • Examine the temporal, nasal, upper, and lower edges of the visual fields of each eye separately
    • Examination of pupillary light reflex
      • Direct pupillary reflex
        • Shining light into one eye causes myosis of that eye
      • Indirect pupillary reflex
        • Shining light into one eye causes myosis of the contralateral eye
    • Examination of oculopalpebral reflex
      • An object quickly approaching the eye elicits blinking
      • Used in unconscious patients (see topic 17)

3. Examination of ocular movements (cranial nerves III, IV and VI)

  • Examination of ptosis
    • Drooping eyelid is due to CN III lesion
  • Examination of diplopia
    • Ask patient whether they have diplopia (double vision)
  • Examination of eye movement
    • Instruct patient to follow your finger as you move it vertically, horizontally, and diagonally
    • Observe for paresis, irregular movement, or nystagmus
    • CN III enables elevation, intorsion, adduction extorsion, and abduction
    • CN IV enables intorsion, depression, and abduction
    • CN VI enables abduction
  • Examination of visual accommodation
    • Instruct patient to follow your finger as you move it toward the patient
    • Miosis, convergence, and accommodation should occur
  • Examination of ciliospinal reflex
    • = pupils dilate if you pinch the skin of the neck
    • Not routinely examined (may be examined in unconscious patients)
    • Absent in Horner syndrome
  • Examination of oculocephalic reflex (Doll’s eye reflex)
    • Used in unconscious patients
    • Absent in brainstem damage
    • Procedure
      • Open patient’s eyes
      • Quickly turn the head to each side
      • Observe the movement of the eyes
    • Negative (reflex is present)
      • Eyes look in the same direction even when the head is turned
      • (Eyes move in the opposite direction as the head)
    • Positive (reflex is absent)
      • Eyes remain in their fixed position, moving as the head moves

4. Examination of the trigeminal nerve

  • Examination of somatosensory function
    • Lightly touch the area of each branch of the trigeminal nerve symmetrically with your thumb and index finger
      • Ophthalmic nerve – eyes and above
      • Maxillary nerve – between eyes and lips
      • Mandibular nerve – lips and below
    • Examine the pain sensation using something sharp in the same way, comparing both sides
  • Examination of motor function
    • Ask: Do you get tired when chewing?
    • Palpate the temporal and masseter muscles while patient opens and closes their mouth
      • They should contract and have normal trophy (size)
  • Examination of corneal reflex
    • Not routinely checked
      • Important in comatose patients, Bell’s palsy, patients with sensory loss on face
    • Touch the patient’s eye with a cotton tip
    • Normally, the patient will blink with both eyes in response
  • Examination of masseter reflex
    • Ask patient to slightly, not completely, open their mouth
    • Place your finger on the patient’s chin and tap your finger with a reflex hammer
    • Normally, the jaw closes slightly in response

5. Examination of the facial nerve. Types of facial palsy.

  • Examination of motor function
    • Inspect for asymmetry
    • Ask patient to:
      • Wrinkle forehead
      • Close eyes tightly
      • Wrinkle nose
      • Inflate cheeks
      • Smile with teeth
      • Whistle
  • Examination of taste sensation
    • From anterior two-thirds of tongue (chorda tympani)
    • Not routinely examined
    • Ask patient whether they have normal taste perception
  • Types of facial palsy
    • Central (supranuclear) facial palsy – forehead is unaffected
    • Peripheral facial palsy – whole face is affected
    • See topic 29

6. Examinations in case of vertigo (n. VIII, central vs. peripheral vestibular lesions)

  • Patients with vertigo should be examined to determine whether the cause is central or peripheral (vestibular)
  • Examination of nystagmus
    • See topic 13
  • Examination of balance
    • Romberg test
      • Procedure:
        • Patient stands and closes their eyes
      • Negative:
        • Balance is just as good (or bad) with eyes closed as with eyes opened
        • This does not necessarily mean that the patient doesn’t sway, just that closing the eyes don’t change the amount of swaying
        • Healthy people will remain stable and not sway
        • People with cerebellar ataxia will sway regardless of eyes open or not
      • Positive:
        • Balance is worse with eyes closed (i.e., balance worsens, or patient starts swaying)
        • Indicates spinal sensory or vestibular problem on the side to which the patient sways
    • Unterberger test
      • Procedure:
        • Ask the patient to walk on the spot with their eyes closed for 30 seconds
      • Negative:
        • Patient does not rotate, or rotates less than 45°
      • Positive:
        • Patient rotates more than 45°
        • Indicates cerebellar or vestibular problem
  • Differentiating central and peripheral causes of vertigo
    • See topic 30

7. Dix-Hallpike and Halmágyi-manoeuvre, alternation cover test and Epley – reposition manoeuvre

  • Dix-Hallpike manoeuvre
    • Used in suspected BPPV
    • Procedure:
      • Patient sits on the examination table
      • Rotate the head 45 degrees to the side of the suspected BPPV
      • Keeping the neck rotated, quickly lay the patient in a supine position so that their head hangs slightly off the short end of the table
      • Hold this position for 20 seconds
      • Slowly reposition patient into the original seated position
    • Negative:
      • Patient experiences no vertigo
      • No nystagmus appears
    • Positive:
      • Patient experiences vertigo and nystagmus when supine, which spontaneously resolve within the 20 seconds
  • (Halmágyi) head impulse test (HIT)
    • Determines whether the vestibuloocular reflex is intact
    • Procedure:
      • Patient sits or stands before you
      • Ask the patient to fix their gaze on your nose
      • Quickly turn the patient’s head to each side 15° multiple times and observe whether the patient loses the visual fixation
    • Negative:
      • Patient maintains visual fixation on your nose
    • Positive:
      • Patient’s eyes “turn away” when turned to the affected side, but is quickly corrected
      • Positive: Vestibular lesion on the affected side
  • Alternating cover test
    • Determines whether there is skew deviation, a sign of central vestibular lesions
    • Procedure:
      • Ask the patient to fix their gaze on your nose
      • Cover one of the patient’s eyes for a while
      • Suddenly move the cover to the other eye
      • Examine the recently uncovered eye for movements
    • Negative:
      • The uncovered eye does not do any corrective movements
    • Positive:
      • The uncovered eye performs a small corrective movement
  • Epley repositioning manoeuvre
    • Indicated if Dix-Hallpike is positive
    • This procedure moves the stone from the posterior semicircular canal into the utricle, improving symptoms
    • Procedure:
      • Patient sits on the examination table
      • Rotate the head 45 degrees to the side of the suspected BPPV
      • Keeping the neck rotated, quickly lay the patient in a supine position so that their head hangs slightly off the short end of the table
      • Hold this position for 30 seconds, or until the nystagmus disappears
      • Turn patient’s head by 90° towards the unaffected side
      • Hold this position for 30 seconds, or until the nystagmus disappears
      • Turn patient’s head another 90° towards the unaffected side, so that the patient is lying on their side with they head facing the ground
      • Hold this position for 30 seconds, or until the nystagmus disappears
      • Slowly bring patient back to a seated, upright position with the head in a neutral position
      • Ask patient to remain in this position for about 15 minutes

8. Examination of nerves IX, X, XI and XII

  • Glossopharyngeal nerve (IX)
    • Mixed sensory, motor, and parasympathetic
      • Motor function is shared with the vagus nerve
    • Examination of the gag reflex
      • Not routinely examined
      • By touching the posterior wall of the pharynx with something
    • Examination of taste sensation
      • From posterior third of tongue
      • Not routinely examined
    • Examination of parasympathetic function
      • Stimulates parotid gland
      • Not routinely examined
  • Vagus nerve (X)
    • Mixed sensory, motor, and parasympathetic
    • Examination of motor function
      • Pharyngeal muscles
        • Ask whether patient has problems swallowing
        • Observe the patient swallowing water
      • Soft palate and uvula
        • Check whether the uvula deviates to one side
          • In a palsy the uvula will deviate to the unaffected side
        • Check for symmetrical movement of soft palate when patient says “aah”
      • Vocal cords
        • Is the patient hoarse?
  • Accessory nerve (XI)
    • Pure motor
      • Trapezius is innervated contralaterally
      • Sternocleidomastoid is innervated ipsilaterally
    • Examination of trapezius function
      • Ask patient to lift their shoulders
      • Apply resistance against the movement
    • Examination of sternocleidomastoid function
      • Ask patient to turn their head
      • Apply resistance against the movement
  • Hypoglossal nerve (XII)
    • Pure motor
    • Examination of tongue muscles
      • Ask patient to protrude the tongue
      • In case of lesion it will deviate to the affected side
    • Examination of tongue trophy
      • Look for atrophy and fasciculations on the tongue
      • In case of lesion it will be apparent on the affected side
    • Examination of tongue spasticity
      • Ask patient to rapidly protrude and retract tongue
      • Observe for spasticity

9. Examination of deep tendon reflexes

  • Radial reflex
    • C5-C6
    • Have patient sit at the edge of the table with their elbow in 90° flexion, palm facing medially
    • Hit the distal, radial part of the forearm with the hammer -> elbow flexion
  • Biceps reflex
    • C5-C6
    • Have patient sit at the edge of the table with their elbow in 90° flexion, palm facing down
    • Hold your finger on the biceps tendon
    • Hit your finger with the hammer -> elbow flexion
  • Triceps reflex
    • C7-C8
    • Have patient sit at the edge of the table with their shoulder abducted
    • Hold the patient’s upper arm for them and ask them to relax the forearm
    • Hit the triceps tendon with the hammer -> elbow extension
  • Patellar reflex
    • L2-L4
    • Have patient sit at the edge of the table with their legs hanging freely
    • Hit the tendon of the quadriceps femoris, just below the patella -> knee extension
  • Achilles reflex
    • S1 – S2
    • Have patient lying on their back
    • Sit next to the patient’s legs, flex the hip and knee
    • Fix the patient’s knee by squeezing it between your upper arm and your torso
    • Hold the patient’s foot in slight dorsiflexion by holding the ball of the foot
      • This puts some tension on the Achilles tendon
    • Hit the Achilles tendon with the hammer -> plantarflexion of ankle
    • Hit the middle of the plantar region of the foot -> plantarflexion of ankle

10. Examination of the pyramidal signs

  • Babinski sign
    • Most important pyramidal sign
    • Procedure:
      • Ask patient to lie on their back
      • Scratch the lateral half of the sole of the foot from bottom to top
      • Response is usually not seen at the beginning of the movement but rather after some centimetres
    • Negative:
      • Plantarflexion, flexion of all toes
    • Positive:
      • Dorsiflexion of the big toe
      • The other toes spread out
  • Triple flexion response/triflexion response
    • Same procedure as for Babinski sign
    • Can be felt more easily with one hand on the quadriceps muscle
    • Negative:
      • Plantarflexion of all toes
    • Positive:
      • Dorsiflexion of foot + flexion of knee + flexion of hip
  • Achilles clonus
    • Procedure:
      • Ask patient to lie on their back
      • Dorsiflex the foot quickly
    • Negative:
      • No clonus in the gastrocnemius
    • Positive:
      • Clonus in the gastrocnemius
  • Patellar clonus
    • Procedure:
      • Ask patient to lie on their back
      • Quickly thrust the patella downwards
    • Negative:
      • No clonus in the quadriceps
    • Positive:
      • Clonus in the quadriceps
  • Hoffman sign
    • Procedure:
      • Hold the PIP joint of the middle finger, stabilizing it
      • Repeatedly flick down the distal phalanx of the middle finger
    • Negative:
      • No flexion of the distal phalanx of the thumb or the index finger
      • Bilateral response may be normal
    • Positive
      • Flexion of the distal phalanx of the thumb or the index finger
  • Trömner sign
    • Procedure:
      • Hold the PIP joint of the middle finger, stabilizing it
      • Suddenly flick the volar aspect of the distal phalanx of the middle finger
    • Negative:
      • No flexion of the distal phalanx of the thumb or the index finger
      • Bilateral response may be normal
    • Positive
      • Flexion of the distal phalanx of the thumb or the index finger

11. Examination of the muscle tone and strength. Signs of central vs. peripheral lesion

  • Examination of muscle tone
    • Muscle tone = resistance to passive movement
    • Both sides should be examined and compared
    • Movements should be performed slowly (to observe for rigidity) and quickly (to observe for spasticity)
    • Elbow
      • Passively flex and extend the patient’s elbow
    • Forearm
      • Passively supinate and pronate patient’s hand
    • Wrist
      • Passively flex and extend the patient’s wrist
    • Hip and knee
      • Passively flex and extend hip and knee
    • See topic 32 for pathological results
  • Examination of muscle strength
    • Muscle strength = maximal force patient can produce during active movement
    • Both sides should be examined and compared
    • Examination of muscle strength of upper limbs
      • Proximal muscles
        • Ask patient to lift their arms up in supinated position and keep them there for 30 seconds while their eyes are closed. Then ask whether their arms feel equally heavy. Observe for pronation and drooping
      • Biceps
        • Ask patient to flex their elbow while you resist the movement
      • Finger muscles
        • Ask patient to make rings with the thumb and the little finger and try to “break” the ring. Repeat with the other four fingers
    • Examination of muscle strength of the lower limbs
      • Ankle
        • Ask patient to dorsiflex and plantarflex against your resistance
      • Ask patient to squat 10 times
        • (If they can’t perform this, ask “do you even lift bro?”)
      • Ask patient to walk 10 steps on their toes
      • Ask patient to walk 10 steps on their heels
    • Graded from 0 to 5 (based on MRC scale)
      • 5 – normal muscle strength
      • (4+ – submaximal movement against resistance)
      • 4 – moderate movement against resistance
      • (4- – slight movement against resistance)
      • 3 – can move against gravity but not against resistance
      • 2 – can move perpendicular to gravity but not against it
      • 1 – visible contraction, but no movement
      • 0 – no visible contraction (plegia)
    • Examine for decreased muscle trophy
      • Observe especially if there are side differences
    • Evaluation
      • Monoparesis = weakness of one limb
      • Hemiparesis = weakness of one side of body
      • Paraparesis = weakness of both legs
      • Tetraparesis = weakness of all limbs
      • (Biparesis = weakness of both arms (super rare))
  • Signs of central vs peripheral lesion
    • See topic 21

12. Examination of Parkinsonism (muscle tone, hypo- and bradykinesia, alternating movements, gait, postural instability)

  • Parkinsonism
    • = A set of symptoms seen in Parkinson disease, Parkinson-plus syndromes, other diseases
    • Examination of muscle tone
      • See topic 11
      • Rigidity is typical for Parkinsonism, especially cogwheel rigidity
    • Examination of bradykinesia
      • Bradykinesia = active movements are slow and have decreased amplitude
      • Observe patient’s active movements for slowness and decreased amplitude
        • Not only slow execution of the movement, but pauses occur too
    • Examination of alternating movements
      • Ask patient to perform quick, alternating movements
        • Touching thumb and index finger and spreading them again, repeatedly
        • Clenching and opening the fist repeatedly
        • Pronating and supinating the hand repeatedly
        • Dorsiflex and plantarflex the foot repeatedly
      • Observe for slowness
      • Negative:
        • Normal movements, no slowness
      • Positive:
        • Bradydiadochokinesia = alternating antagonistic movements are performed slowly
    • Examination of gait
      • Ask patient to walk
      • Negative:
        • Normal gait
      • Positive:
        • Short, narrow-based steps
        • Pauses when turning around
    • Examination of postural instability
      • Ask patient if they have had falls or experience postural instability
      • Pull test
        • Ask patient to stand upright
        • Pull the patient’s shoulders gently from behind
        • Observe the patient’s ability to regain their posture
        • Negative:
          • Can regain posture with 1 – 2 steps
        • Positive:
          • Posture only regained with 3 or more steps, or patient needs help to regain balance
    • Examination of tremor
      • Observe for tremors during rest and during active movements
      • Rest tremor is characteristic of Parkinson disease
    • See also topic 39

13. Examination of the cerebellar symptoms

  • Symptoms manifest on the same side as the lesion
  • Cerebellar ataxia
    • Gait ataxia
      • Wide-based, unsteady gait
      • Similar to the gait of drunk people
      • Observe patient’s gait
      • Observe whether the gait worsens or stays the same when patient closes their eyes
        • Worsening with eyes closed suggest sensory ataxia
        • Cerebellar gait ataxia does not worsen with closed eyes
      • Negative/inconclusive Romberg test
      • Positive Unterberger test (topic 6)
    • Limb ataxia
      • = uncoordinated movement of the limbs
      • Finger-to-nose test usually positive
      • Heel-to-shin test
        • Procedure
          • Ask patient to lie flat on their back
          • Ask them to place one heel on the opposite knee, and then move the heel smoothly down the shin to the ankle
          • Repeat on the opposite side
        • Negative:
          • Patient can perform the movement smoothly
        • Positive:
          • Patient is unable to perform the movement smoothly. Tremors appear
    • Trunk ataxia
      • = inability to sit or stand upright without support
      • Positive Romberg test (topic 6)
  • Dysmetria
    • = overshooting or undershooting the intended movement
    • Finger-to-nose test
      • Procedure
        • Hold your finger out in front of the patient
        • Ask the patient to touch their nose, then your finger
        • Repeat this movement as you move your finger to new positions
      • Negative:
        • Patient can do movement normally, touching your finger every time
      • Positive:
        • Patient will miss your finger due to constantly overshooting or undershooting the precise movements
  • Dysdiadochokinesia
    • = alternating antagonistic movements are irregular, uncoordinated
    • Ask patient to perform quick, alternating movements
      • Touching thumb and index finger and spreading them again, repeatedly
      • Clenching and opening the fist repeatedly
      • Pronating and supinating the hand repeatedly
      • Dorsiflex and plantarflex the foot repeatedly
    • Observe for irregularity and uncoordinated movements
  • Dysarthria
    • = scanning speech
    • Words are broken down into separate syllables
    • See topic 16
  • Intention tremor
    • = broad, coarse, slow tremor which occurs during purposeful movement
    • Tremor is at its worst right before reaching the target
    • Observed during finger-to-nose test
    • See also topic 33
  • Examination of nystagmus
    • Try to provoke nystagmus by eliciting ocular movements
    • Does the patient have nystagmus?
    • Describe the type of the nystagmus
      • Horizontal/vertical/rotatory/combined
    • Which direction is the nystagmus?
      • The direction is named after the fast component
      • The nystagmus is directed toward the side of the lesion
    • Does visually fixating the gaze suppress the nystagmus?
      • Fixation does not improve nystagmus of cerebellar origin
    • See also topic 30

14. Examination of the sensation

  • Compare both sides
  • Show and tell the patient about the examination before you perform it with their eyes closed
  • Examination of fine touch
    • Pathway: dorsal column
    • Procedure
      • Ask patient to close their eyes
      • Touch patient softly with finger or cotton pad
      • Tell patient to tell you when they feel it
    • Positive:
      • Hypoesthesia: decreased sensation
      • Anaesthesia: no sensation
      • Allodynia: painful sensation for a non-painful stimulus
  • Examination of vibration
    • Pathway: dorsal column
    • Procedure
      • Hit a tuning fork and place it on the patient’s forehead, so they have a reference
      • Ask patient to close their eyes
      • Hit the fork again and place it on a bony prominence in the area to be examined
    • Positive:
      • Decreased or absence of vibration sensation
  • Examination of proprioception (joint position)
    • Pathway: dorsal column
    • Procedure
      • Ask patient to close their eyes
      • Hold the patient’s hallux
      • Move the distal joint up and down randomly, and ask the patient at random times to identify the change in position
      • Perform the same movement for the 4th finger
    • Positive:
      • Decreased or absence of joint movement sensation
    • Note: Joint position sense is extremely sensitive, so even small movements can be felt by the patient
  • Examination of pain sensation
    • Pathway: spinothalamic tract
    • Procedure
      • Ask patient to close their eyes
      • Prick the patient’s skin with a pointed object
    • Positive
      • Analgesia: No pain sensation
      • Hypoalgesia: Decreased pain sensation
      • Hyperalgesia: Increased pain sensation

15. Examination of the limb- and trunk ataxia

  • See topic 13

16. Examination of the speech and the main types of disturbances

  • Examination of speech
    • The speech can be examined while taking the history
  • Main types of disturbances of speech
    • Dysphonia
      • Abnormal quality of voice
      • Due to mechanical abnormality of vocal cords
      • Examples
        • Laryngitis -> Hoarseness
        • Common cold -> nasal voice
    • Dysarthria
      • Abnormal articulation
      • Due to lesion to nervous pathways or muscles responsible for articulation
      • Examples
        • LMN lesion of soft palate -> paralytic dysarthria
          • (Nasal voice)
        • Spasticity of tongue, palate -> spastic dysarthria
          • (sounds like patient is talking with a plum in their mouth)
        • Cerebellar disease -> cerebellar dysarthria/scanning speech
        • Parkinsonism -> extrapyramidal/hyphonic dysarthria
          • (Slow, soft, monotonous)
    • Dysphasia/aphasia
      • Impaired language, either speaking or understanding
      • Due to hemispheric lesions
      • See topic 36

17. Examination of the unconscious patient

  • Differentiate between cardiac, metabolic, and neurological causes
    • Most unconscious patients have underlying cardiac or metabolic problem; neurologic cause of unconsciousness is rare
    • Cardiac causes of unconsciousness
      • Most common
      • Suspicious features
        • Low heart rate
        • Low blood pressure
        • Abnormal ECG
    • Endogenous metabolic causes of unconsciousness
      • Etiology
        • Metabolic acidosis
        • Hypoglycaemia
        • Hyperglycaemic crisis
        • Hepatic encephalopathy
        • Uraemia
        • Hypercapnia
      • Suspicious features
        • Abnormal blood sugar
        • Kussmaul breathing (quick and deep)
        • Abnormal odour of breath
        • Hypotonia
        • Hyporeflexia
    • Exogenous metabolic causes of unconsciousness (intoxication)
      • Etiology
        • Opioids
        • Benzodiazepines
        • Alcohol
      • Suspicious features
        • Drugs or needles around the patient
        • Needle marks on the patient’s arms
        • Slow, superficial breathing
        • Extreme miosis (pinpoint pupils)
        • Low blood pressure
    • Neurological causes of unconsciousness
      • Etiology
        • Brainstem lesion (of the ascending reticular activating system)
          • Increased ICP -> foramen magnum herniation
          • Brainstem stroke
          • Trauma
        • Bilateral thalamus lesion
          • There’s a relatively frequent malformation where both thalami receive blood from same artery -> prone to bilateral ischaemia
        • Bilateral frontal lobe lesion
      • Suspicious features
        • Abnormal pupillary light reflex
          • Unilateral dilated fixed pupil – CN III palsy
          • Bilateral dilated fixed pupils – tectal lesion or atropine
          • Midpoint fixed pupils – midbrain lesion
          • Pinpoint fixed pupils – pons lesion, opioids
          • Small reactive pupils – thalamus lesion or metabolic
        • Abnormal conjugation
          • Conjugated and deviated eyes (deviate ipsilateral to cortical lesion)
          • Dysconjugated eyes (brainstem or CN III, IV, VI lesion)
          • Skew deviation (brainstem lesion)
        • High blood pressure
          • Increased ICP -> Cushing reflex
        • Decorticate posturing
          • Flexed elbows, adducted arms, flexed fingers and wrists
          • Indicates damage above the red nucleus, e.g. rostral midbrain, thalamus, internal capsule, hemispheres
        • Decerebrate posturing
          • Upper and lower extremities extended and internally rotated
          • Indicates damage below the red nucleus, e.g. caudal midbrain or pons
        • Absent oculocephalic reflex (brainstem lesion) (see topic 3)
        • Absent corneal reflex
        • Absent cough reflex (lower brainstem lesion)
        • Hyperreflexia
  • History
    • From relatives or other witnesses
    • Did patient have any symptoms right before loss of consciousness?
    • Was loss of consciousness abrupt or gradual?
    • Patient’s recent health
    • Patient’s functional status
    • Previous medical history
    • Medication use
  • Examination
    • General examination
      • ABC (airways, breathing, circulation)
        • Are the airways obstructed?
        • Breathing
          • Cheyne-Stokes breathing -> brainstem lesion, heart failure
          • Slow, superficial breathing -> drugs, narcotics
          • Quick, superficial breathing -> brainstem lesion
          • Kussmaul breathing -> acidosis, hyperglycaemic crisis
        • Circulation
          • Pulse
          • Temperature
            • Hyperthermia -> infection, heat stroke
            • Hypothermia -> cold exposure, sepsis, CNS disease
          • Skin colour
          • Blood pressure
            • Hypertension -> CNS haemorrhage
            • Hypotension -> circulatory shock
      • Smell of breath
        • Alcohol, ketone bodies, liver failure, uraemia, …
      • Bruises which can suggest a fall
    • Neurological examination
      • Determine Glasgow coma scale score
        • To what degree is the patient arousable?
          • Shout to them
          • Induce pain
            • Press on the exit point of the ophthalmic nerve
            • Press on fingernail
        • Observe eye opening, movement, and verbal response
      • Examination of meningeal signs (see topic 1)
        • Only examined if cervical trauma can be excluded
        • Meningeal signs can be present in subarachnoid haemorrhage
      • Examination of cough reflex
        • By suction or inserting endotracheal tube
      • Examination of pupil and pupillary reflexes
        • Unilateral, maximally dilated
        • Bilateral, maximally dilated
        • Mid-dilated, does not react to light
        • Tiny pinpoint pupils
        • Horner syndrome (see topic 41)
      • Examination of position of eyes
        • Conjugate deviation
        • Dysconjugate deviation
        • Skew deviation
      • Examination of spontaneous eye movements
        • Downward deviation of eyes
        • Repetitive horizontal movements
      • Examination of reflex eye movements
        • Oculocephalic (doll’s eyes) reflex
        • Oculovestibular reflex
      • Examination of corneal reflex
      • Examination of muscle tone
      • Examination of fundus
        • Papilloedema
        • Haemorrhage
      • Examination of pyramidal signs

18. Examination of the patient after a short-time loss of consciousness

  • Differentiate between syncope and neurological causes
    • 90% are non-neurological
    • Syncope
      • Causes
        • Cardiac syncope
        • Reflex syncope
        • Autonomic dysfunction
        • Recent change in drugs
      • Suspicious features
        • Prodromal symptoms
          • Blurry vision, sight goes dark
          • Sweating
        • Lasts seconds
        • Patient is oriented immediately after
    • Neurological causes
      • Almost always seizures
      • Suspicious features
        • Prodromal symptoms
          • Often sudden blackout, no prodromal symptoms
          • Aura
        • Lasts minutes
        • Enuresis
        • Muscle soreness
        • Bitten tongue on lateral part
        • Patient has postictal period of tenebrosity and disorientation after
  • History
    • Precipitating factor
    • Did the patient feel the episode coming?
    • What the patient was doing
    • How long did the episode last?
      • Seconds -> non-neurological
      • Minutes -> neurological
    • Did the patient bite his tongue?
      • Indicates seizure
    • Did the patient lose continence?
      • Indicates seizure
    • Did the patient regain full consciousness immediately or was it gradual?
      • A lasting post-ictal confusion is suggestive for a seizure
      • In true syncope full consciousness is immediately regained
    • Previous loss of consciousness
    • Drugs
      • Antidiabetics
      • Antihypertensives
    • Family history
    • Previous medical history
      • Diabetes
      • Hypothyroidism
      • Epilepsy
      • Known heart problems
    • Recent hydration status
  • Examination of blood glucose
  • Examination of cardiovascular system
    • Electrocardiogram
    • Heart auscultation
    • Turgor
  • Neurological examination
    • Inspect for trauma

19. Examination of the patient with dementia

  • (No good source, uncertain what it important)
  • History
    • An informant who knows the patient well should be present
      • When did the informant first notice memory loss?
      • How has the memory loss progressed since then?
      • Recent changes in personality or mood?
    • Drugs
      • Opioids
      • Anticholinergics
      • Antidepressants
      • Sedatohypnotics (benzos, etc.)
    • Which daily activities can the patient perform now compared to previously?
    • Medical history
      • Stroke/TIA
      • Cardiovascular disease
      • Diabetes
    • Alcohol use
    • Sleep status
    • Other neurological symptoms
      • Loss of vision
      • Loss of motor function
      • Tremor
      • Poor balance and falls
      • Incontinence
  • Cognitive testing
    • MMSE (mini mental state examination)
    • WAIS (Wechsler adult intelligence scale)
  • Laboratory examination
    • B12 deficiency
    • Thyroid status
  • Imaging
    • In cases of acute neurologic deterioration
    • Head CT or MRI
  • Neurological physical examination
    • Examination for frontal release signs
      • See topic 54
    • Ocular examination (topics 2 and 3)
    • Examination of gait
    • Examination of extrapyramidal symptoms
      • Bradykinesia, rigidity, dystonia, akathisia, etc.
      • -> Dementia with Lewy bodies, Parkinson, vascular dementia, etc.
    • Examination of pyramidal signs
      • -> motor neuron disease
    • Examination of fundus
      • Papilloedema -> tumour, hydrocephalus

20. Examination of the confused patient

  • ?
  • No source

“B” Theoretical background of physical examination

21. Typical symptoms of peripheral and central lesions

Peripheral lesion Central lesion
Muscle strength Decreased Decreased
Muscle tone Decreased (flaccidity) Increased (spasticity)
Muscle trophy Decreased (atrophy) Normal (decreased in the chronic phase)
Fasciculations Present Absent
Deep tendon reflexes Decreased or absent Brisk or increased
Pyramidal signs Absent Present
Sensory loss Absent or present in the distribution of one nerve root, plexus or peripheral nerve Absent or present in the hemi-, para-, or tetra- patterns, or in niveau pattern if spinal cord is affected

22. Symptoms of nuclear and supranuclear lesions

  • Nuclear lesion (bulbar palsy)
    • = bilateral lesion of the motor nucleus of a cranial nerve, its axon, or its NMJ
    • Pathophysiology
      • Cranial nerves IX, X, XI, and XII are affected
      • Equals a “lower motor neuron” lesion, with typical peripheral motor lesion symptoms like atrophy and flaccidity
    • Clinical features
      • Normal facial expressions (because VII is unaffected)
      • Nasal speech
      • Dysphagia of fluids
      • Atrophic and fasciculating tongue
      • Absent gag reflex
  • Supranuclear lesion (pseudobulbar palsy)
    • = bilateral lesion of the corticobulbar tracts
    • Pathophysiology
      • Cranial nerves V, VII, IX, X, XI, XII are affected
      • Equals an “upper motor neuron” lesion, with typical central motor lesion symptoms like spasticity and hyperreflexia
    • Clinical features
      • Stiff, spastic facial muscles -> no facial expressions
      • Spastic dysarthria (Donald Duck voice)
      • Dysphagia
      • Spastic tongue
      • Pseudobulbar affect/emotional incontinence
        • Uncontrollable laughing or crying
        • Think Joaquin Phoenix in the Joker
      • CN V palsy -> exaggerated jaw jerk reflex
      • Brisk gag reflex

23. Symptoms of anterior-territory stroke

  • Anterior territory stroke = stroke involving the territory of the internal carotid system, including the anterior and middle cerebral arteries
    • Middle cerebral artery infarct is most common, 2/3 of all strokes
    • Anterior cerebral artery infarct is rare, ~2% of all strokes
  • Contralateral hemiparesis
  • Contralateral hemisensory loss
  • Contralateral homonymous hemianopia
  • Aphasia (if dominant hemisphere is affected)
  • Contralateral hemineglect (if nondominant hemisphere is affected)
  • Gaze deviation toward side of lesion
  • Amaurosis fugax
    • Sudden, painless loss of vision
    • Lasts for second to minutes but recovers spontaneously
    • Usually unilateral

24. Symptoms of posterior-territory stroke

  • Posterior territory stroke = stroke involving the territory of the vertebrobasilar arterial system, including
    • 20% of stroke cases
  • Ipsilateral limb ataxia
  • Ipsilateral Horner syndrome
  • Cranial nerve involvement
    • Ipsilateral diplopia
    • Ipsilateral facial sensory loss
    • LMN facial palsy
    • Vertigo
    • Dysphagia
    • Dysarthria
  • Contralateral or bilateral hemiparesis
  • Contralateral or bilateral hemisensory loss
  • Homonymous hemianopia
  • Cortical blindness
    • = Blindness with an otherwise normal ophthalmological examination

25. Symptoms of brainstem alternating syndromes (Weber’s and Wallenberg’s syndrome)

  • Brainstem alternating syndromes
    • Syndromes caused by brainstem lesions characterised by ipsilateral motor and nuclear symptoms, and contralateral sensory symptoms
    • Our teacher said we only need to know Wallenberg
  • Wallenberg syndrome (= lateral medullary syndrome)
    • Infarct of lateral part of medulla oblongata due to posterior inferior cerebellar artery (PICA) obstruction
    • Affection of ipsilateral cerebellar peduncle -> ipsilateral hemiataxia
    • Affection of ipsilateral lateral spinothalamic tract, which later crosses in the anterior white commissure
      • -> Contralateral hypoesthesia
      • -> Contralateral decreased temperature sensitivity
    • Affection of ipsilateral vestibular nuclei
      • -> vertigo, nausea
      • -> dizziness
      • -> ipsilateral nystagmus
    • Affection of ipsilateral nucleus ambiguus (IX, X, XI)
      • -> Dysphagia
      • -> Hoarseness
      • -> Hiccups
    • Affection of spinal trigeminal nucleus (V)
      • -> Ipsilateral hypoesthesia of the face
      • -> Ipsilateral decreased temperature sensitivity of the face
    • Affection of sympathetic fibres -> Ipsilateral Horner syndrome
  • Weber syndrome (= ventral midbrain syndrome)
    • Affection of ventral midbrain due to posterior cerebral artery obstruction
    • Affection of ipsilateral oculomotor nerve
      • -> ptosis
      • -> mydriasis
      • -> inferolateral gaze deviation
    • Affection of ipsilateral corticospinal tract, which later crosses in the pyramidal decussation
      • -> Contralateral hemiparesis or plegia
    • Contralateral parkinsonism

26. Symptoms of dissociative sensory loss

  • Dissociated sensory loss
    • = pattern of sensory loss caused by lesion of a single tract, resulting in the loss of either the spinothalamic tract or the dorsal column, but not both
  • Lesion of spinothalamic tract with intact dorsal column
    • Occurs in anterior cord syndrome, central cord syndrome, conus medullaris syndrome
    • -> loss of pain and temperature sensation
  • Lesion of dorsal column with intact spinothalamic tract
    • Occurs in posterior cord syndrome
    • -> loss of fine touch, sensation of vibration, and proprioception
  • See also topic 42

27. Types of visual field defects

  • Terms
    • Homonymous vision loss = same region is lost on both eyes
      • E. g. temporal half on left eye and nasal half on right eye
    • Heteronymous vision loss = opposing regions are lost
      • E. g. temporal half on left eye and temporal half on right eye
    • Hemianopia = loss of half the vision field
    • Quadrantanopia = loss of one quarter of the vision field
  • Complete unilateral vision loss
    • Due to pre-chiasmal lesion (retina or optic nerve)
  • Bitemporal heteronymous hemianopia
    • = bilateral loss of temporal visual field
    • Due to lesion of the middle part of the optic chiasm
    • Fibres transmitting the temporal part of the visual field crosses in the optic chiasm
    • Fibres transmitting the nasal part of the visual field does not cross
  • Ipsilateral nasal hemianopia
    • = ipsilateral loss of nasal visual field
    • Due to lesion of the lateral part of the optic chiasm
  • Binasal heteronymous hemianopia
    • = bilateral loss of nasal visual field
    • Due to lesion of both lateral parts of the optic chiasm
  • Contralateral homonymous hemianopia
    • = loss of the ipsilateral nasal and contralateral temporal visual fields
    • Due to lesion of the optic tract
    • The optic tract transmits information from the ipsilateral nasal visual field and the contralateral temporal visual field
  • Contralateral homonymous upper quadrantanopia
    • = loss of ipsilateral upper nasal quadrant and contralateral upper temporal quadrant
    • Due to lesion of
      • Anterior part of optic radiation
      • Lower part of calcarine fissure
  • Contralateral homonymous lower quadrantanopia
    • = loss of ipsilateral lower nasal quadrant and contralateral lower temporal quadrant
    • Due to lesion of
      • Posterior part of optic radiation
      • Upper part of calcarine fissure
  • Contralateral homonymous hemianopia with central sparing
    • = loss of the ipsilateral nasal and contralateral temporal visual fields, but the central vision remains intact
    • Due to lesion of the occipital lobe

28. Types of gaze palsies: nuclear and supranuclear gaze palsy, internuclear ophthalmoplegia

  • Gaze palsy = limitation of voluntarily moving both eyes in the same direction across the midline
    • Can be nuclear or supranuclear in origin
    • Due to lesion of the
      • Cortical gaze centre -> supranuclear
      • Brainstem gaze centre -> nuclear
      • The connections between them -> supranuclear
    • Supranuclear gaze palsy -> movement can still be elicited by reflex eye movements (oculocephalic reflex, caloric testing)
    • Nuclear gaze palsy -> movement cannot be elicited by reflexes
  • Horizontal gaze palsy = eyes can’t be moved in one or both of the horizontal directions
    • Most common gaze palsy
    • Etiology
      • Stroke in pons
  • Vertical gaze palsy = eyes can’t be moved in one or both of the vertical directions
    • Etiology
      • Stroke in midbrain
      • Pinealoma
      • Multiple sclerosis
  • Downward gaze palsy = eyes can’t be moved downward, other directions ok
    • Etiology
      • Progressive supranuclear palsy
  • Internuclear ophthalmoplegia
    • = lesion of one or both medial longitudinal fasciculi
    • Can be considered as a supranuclear gaze palsy
    • Etiology
      • Multiple sclerosis
      • Stroke
      • Brainstem tumor
    • Clinical features
      • Impaired adduction of the ipsilateral eye
      • Abduction nystagmus of the contralateral eye
      • One or both eyes can be affected

29. Symptoms of peripheral and central facial palsy

  • Innervation of facial muscles
    • Upper half of facial muscles are innervated by fibres from both hemispheres
      • Muscles for movement of forehead and eyelid
    • Lower half is innervated only from contralateral hemisphere
  • Central facial palsy
    • Etiology
      • Stroke
      • Tumour
    • Clinical features
      • All symptoms on contralateral side
      • Frowning, eye-closing, blinking is normal
      • Drooping corner of mouth
      • Disappearance of nasolabial fold
  • Peripheral facial palsy
    • 50% of all facial palsies are idiopathic and peripheral
    • Etiology
      • Idiopathic (= Bell’s palsy)
      • Lyme disease
      • Otitis media
      • Trauma
    • Clinical features
      • All symptoms on ipsilateral side
      • Frowning, eye-closing, blinking is abnormal
      • Inability to close the eye
      • Drooping corner of mouth
      • Disappearance of nasolabial fold
      • Pain in ear
      • Hyperacusis

30. Characteristic appearance of harmonic and disharmonic vestibular syndromes

  • Harmonic vestibular syndrome = peripheral vertigo, disharmonic = central vertigo
    • (Try finding a non-Hungarian source which uses these terms)
Peripheral (harmonic vestibular syndrome) Central (disharmonic vestibular syndrome)
Nystagmus direction Never changes direction

Slow component toward affected ear

Direction may change based on gaze

Slow component away from affected ear

Nystagmus type Horizontal or combined horizontal and rotational

Never purely rotational or purely vertical

Any direction

Purely vertical or purely rotational is always central

Sense of motion Severe, nausea common Usually mild
Romberg test Patient falls toward opposite side of the fast component of the nystagmus Patient falls toward same side as the fast component of the nystagmus
Does visual fixation suppress nystagmus? Yes No
Postural instability Instability toward affected side

Walking usually preserved

Severe instability

Walking usually difficult

Other inner ear symptoms (hearing loss, tinnitus) May be present Usually not present
Ataxia, diplopia, dysphagia, weakness, other neurological symptoms Absent Often present

31. Pyramidal signs and assessment

  • Pyramidal signs are those which refer to a lesion of the pyramidal (corticospinal) tract
  • Hyperreflexia (= increased reflex response) and spasticity are generally seen in pyramidal lesions but is not specific
  • Presence of pyramidal signs in infants is physiological
  • See topic 10
  • Babinski sign
    • Most important pyramidal sign
    • Specific but not sensitive
  • Triflexion response
  • Achilles clonus

32. Alterations of muscle tone, types, and clinical appearance

  • Hypotonia (flaccidity) = decreased muscle tone
  • Spasticity
    • = Increased resistance to passive movement, but the resistance is smaller when the movement is performed quickly
      • Velocity-dependent resistance to movement
    • Classically manifests as clasp knife phenomenon = At the beginning of the movement there is increased resistance to passive movement, but the resistance suddenly decreases
    • Spasticity is better observed when passive movement is performed quickly
    • Best observed in the flexors of the upper extremity and extensors of lower extremity
    • Seen in upper motor neuron lesions
  • Rigidity
    • = Increased resistance to passive movement throughout the whole movement
      • Velocity-independent resistance to movement
    • Rigidity is better observed when passive movement is performed slowly
    • Seen in parkinsonism and neuroleptic malignant syndrome
  • Cogwheel rigidity
    • = rigidity which sets in and releases multiple times throughout the movement
    • Muscles “jerk” throughout the movement
    • Specific for Parkinson
  • Paratonia (= gegenhalten)
    • Resistance to movement like rigidity, but the resistance decreases when the patient is distracted, indicating a psychological component
    • Seen in dementia and anxious people

33. Pathological tremors, types, and examinations

  • Postural tremor
    • = tremor which occurs when arms are held out against gravity
    • Physiological tremor
      • Etiology
        • Stress
        • Sympathetic activation
        • Hyperthyroidism
        • Caffeine
        • Alcohol withdrawal
      • Clinical features
        • Fine tremor
    • Essential tremor
      • Etiology
        • Hereditary (autosomal dominant)
      • Clinical features
        • Fine tremor
        • Affects the hands in 90% of cases
        • Tremor of vocal cord can cause “shaky” voice
        • Worsens with stress, fatigue, caffeine
        • Improves with alcohol
  • Intention tremor
    • Due to cerebellar injury
    • Etiology
      • Cerebellar stroke
      • Trauma
      • Multiple sclerosis
      • Chronic alcohol abuse
    • Clinical features
      • Occurs during voluntary movements
      • Coarse (low frequency) tremor
      • Slow “zigzag” movement towards a target
      • Tremor is biggest right before reaching target
  • Resting tremor
    • Etiology
      • Parkinsonism
      • Neuroleptic drugs
    • Clinical features
      • Occurs during rest
      • Special movement of the thumb and index finger as if you were rolling a pill between them (pill-rolling tremor)
  • Psychogenic tremor
    • Etiology
      • Psychiatric disease
    • Clinical features
      • Features change when patient is distracted
  • Flapping tremor (asterixis)
    • Etiology
      • Hepatic encephalopathy
    • Clinical features
      • Characteristic “flapping” motion of hands

34. Types of gait disturbances

  • Antalgic gait
    • Etiology
      • Pain in limb
    • Clinical features
      • Limping
      • Reduces weight on painful limb
  • Steppage gait
    • Etiology
      • Lesion of peroneal nerve
      • Polyneuropathy
    • Clinical features
      • Foot drops while walking
      • Knees raised high to compensate
  • Trendelenburg gait
    • Etiology
      • Weakness of gluteus medius
    • Clinical features
      • Patient is unable to hold hip horizontal when standing on one foot
      • Hip drops toward weak side during walking -> “waddling” gait
  • Spastic gait
    • Etiology
      • Upper motor neuron lesion
    • Clinical features
      • Lower limb kept in extension on affected side, circumduction instead
        • Circumduction = Leg makes a half-circle
      • Upper limb kept in flexion on affected side
  • Scissoring gait
    • Etiology
      • Bilateral upper motor neuron lesion (Cerebral palsy)
    • Clinical features
      • When walking knees and thighs cross in a scissor-like movement
  • Vestibular gait
    • Etiology
      • Vestibular disease
    • Clinical features
      • Direction deviates toward side of lesion
  • Sensory ataxic gait
    • Etiology
      • Sensory dysfunction due to peripheral neuropathy or dorsal column disease
    • Clinical features
      • Tottering, wide-based gait
      • Worsens with eyes closed
  • Cerebellar ataxic gait
    • Etiology
      • Cerebellar disease
    • Clinical features
      • Tottering, wide-based gait
      • Does not worsen with eyes closed
      • Similar to the gait of drunk people
  • Hypokinetic/parkinsonian gait
    • Etiology
      • Parkinson disease
    • Clinical features
      • Narrow-based gait
      • Small, shuffling steps
      • Slow, many pauses
      • Hesitation to start walking
      • “En bloc” turning (= turning with many small steps)
  • Dyskinetic gait
    • Etiology
      • Dystonia
      • Chorea
    • Clinical features
      • Gait is accompanied by many involuntary movements
  • Apraxic gait / gait apraxia
    • Etiology
      • Frontal lobe disease
      • Dementia
      • Normal pressure hydrocephalus
    • Clinical features
      • Wide-based gait
      • Inadequate synergy
      • Hesitation to start walking
      • Patient can coordinate legs when lying down but not when walking
  • Psychogenic gait
    • Etiology
      • Psychiatric disease
    • Clinical features
      • Bizarre features, varying from patient to patient
      • The features change if patient’s attention is diverted

35. Types of apraxia

  • Apraxia = inability to complete skilled motor movements despite intact power
    • Due to decreased cortical function causing difficulty in performing targeted, voluntary movements
  • Ideational apraxia
    • = patient is unable to perform complicated series of movements
    • An abnormality of motor planning
    • Examples:
      • Can’t squeeze toothpaste onto a toothbrush
      • Problems dressing, eating, bathing
      • Patient puts socks on top of shoes
      • Patient dries to drink out of bottle without removing cap
    • May indicate damage to parietal lobe of dominant hemisphere
  • Ideomotor apraxia
    • = patient can plan to how to perform tasks, but is unable to carry them out, especially when trying to imitate the doctor’s movements
    • Examples:
      • Patient can’t imitate blowing out a candle, waving goodbye, etc.
      • Patient can’t pick coins out of hand and insert into vending machine
    • May indicate damage to parietal lobe of dominant hemisphere
  • Constructional apraxia
    • = patient can orient and act in two-dimensional system but not in three-dimensional system
    • Examples
      • Patient can’t manage an inside-out dress
      • Patient can’t draw three-dimensional objects
  • Apraxic gait
    • See topic 34

36. Types of aphasia

  • Aphasia = patient is unable to speak and/or understand speech
    • But patient is alert, can hear, could previously speak, and innervation of vocal cord is normal
  • Broca aphasia (motor aphasia)
    • Due to damage to Broca area in the frontal lobe of the dominant hemisphere
    • Patient:
      • Can’t form grammatically correct speech and
      • Can’t repeat sentences
      • Can comprehend speech
      • Is usually aware of this, which makes them frustrated
  • Wernicke aphasia (sensory aphasia)
    • Due to damage to Wernicke area in the temporal lobe of the dominant hemisphere
    • Patient:
      • Can form grammatically correct speech, but it lacks sense
      • Can’t repeat sentences
      • Has problem comprehending speech
      • Has problem with reading and writing
      • Is usually unaware of this
  • Global aphasia
    • Due to damage of both Wernicke and Broca area or the connection between them
    • Patient:
      • Can’t produce speech at all
      • Can’t repeat sentences
      • Has problem comprehending speech
  • Anomic aphasia
    • Patient can’t recall specific names of objects or other specific words, but speech and comprehension are otherwise normal

37. Types of agnosia

  • Agnosia = inability to recognize sensory stimuli, despite a normal sensory system
    • Indicates cortical damage
  • Visual agnosia
    • Person is unable to recognize objects by vision
  • Prosopagnosia
    • Person is unable to recognize faces, often their own face too
      • Ability to identify others based on other cues (clothes, voice, gait) is intact
  • Tactile agnosia
    • Person is unable to recognize objects by touching them
  • Anosognosia
    • Person is unaware that that they have motor or sensory impairment of one side
    • Most commonly due to right parietal lesion, causing anosognosia of left limbs

38. Neglect syndromes

  • Hemineglect = impaired ability to perceive and respond to stimuli from one side
    • Hemineglect of the side contralateral to the lesion
    • Due to damage to the non-dominant hemisphere
      • Because the left hemisphere is dominant in most people, hemineglect almost always occurs on the left side
      • Most frequently due to infarct of right middle cerebral artery area -> left hemineglect
    • Sensory neglect
      • Patient ignores sensory stimulus coming from the side
    • Motor neglect
      • Patient does not spontaneously move limb of affected side
      • Patient may be able to move it when instructed to
    • Hemispatial neglect
      • If patient is asked to draw a clock face, they will omit the side of the clock corresponding to the affected side

39. Characteristic signs of Parkinsonism

  • See also topic 12
  • Characteristic signs of Parkinsonism
    • Rigidity
      • Especially cogwheel rigidity
    • Bradykinesia
      • = active movements are slow and have decreased amplitude
    • Bradydiadochokinesia
      • = alternating antagonistic movements are performed slowly
      • For example, touching the thumb and index finger and spreading them again, repeatedly
    • Hypokinetic gait
      • Narrow-based gait
      • Small, shuffling steps
      • Slow, many pauses,
      • Hesitation to start walking
      • “En bloc” turning (= turning with many small steps)
    • Postural instability
    • Resting tremor

40. Signs of cerebellar lesions

  • See topic 13

41. Horner’s syndrome

  • Horner syndrome
    • Etiology
      • Idiopathic (most cases)
      • Pancoast tumour
      • CNS tumour
      • Brainstem stroke
        • Wallenberg syndrome
      • Internal carotid artery dissection
    • Characteristic triad
      • Loss of sweating on face (anhidrosis)
      • Partially drooping upper eyelid (ptosis)
      • Miosis
    • Absent ciliospinal reflex (topic 3)

42. Types of spinal cord lesions (complete cross section, dorsal column lesion, anterior spinal artery syndrome)

  • According to level of lesion
    • C4 or above -> respiratory paralysis
    • Th1 or above -> tetraparesis
    • Th6 or above -> potential for neurogenic shock
    • S2 – Th1 -> paraparesis
  • Complete cord transection
    • = injury to all regions of spinal cord
    • Etiology
      • Trauma
      • Multiple sclerosis
      • Myelitis
    • Clinical features
      • Bilateral incomplete or total absence of sensory and motor function below lesion
        • Niveau formation at the level of the lesion with anaesthesia below niveau
        • Spastic weakness below level of lesion
      • Loss of autonomic function below level of lesion
        • Bladder incontinence
        • Constipation
  • Brown-Sequard (hemicord) syndrome
    • (not in the topic list so probably not important)
    • = hemisection (section of lateral half) of the spinal cord
      • Most commonly in cervical cord
    • Etiology
      • Penetrating injury
      • Crush injury
    • Pathomechanism
      • The spinothalamic tract crosses in the anterior white commissure of the spinal tract, so it’s affected on the contralateral side
      • The dorsal column crosses in the medulla oblongata, so it’s affected on the ipsilateral side
    • Clinical features
      • Ipsilateral loss of dorsal column modalities below the level of the lesion:
        • Loss of proprioception,
        • Loss of sense of vibration
        • Loss of tactile discrimination
      • Contralateral loss of spinothalamic modalities below the level of the lesion:
        • Loss of pain sensation
        • Loss of temperature sensation
        • Loss of crude touch sensation
      • Ipsilateral spastic paralysis below the level of the lesion
      • Autonomic function often normal
  • Central cord syndrome
    • (not in the topic list so probably not important)
    • = injury to central region of spinal cord
    • Etiology
      • Syringomyelia
      • Hyperextension injury
    • Pathomechanism
      • Most commonly affects cervical spinal cord
      • Spinothalamic tract crosses in the anterior commissure, which lies in the central part of the spinal cord, so injury to this region could damage the crossing spinothalamic tract -> dissociated sensory loss of the adjacent dermatomes (those which cross at the level of the injury)
        • = “suspended sensory loss”
        • Dermatomes above and below the level of the injury are unaffected
      • Corticospinal tract of upper extremities runs closer to the centre than that of the lower extremities -> upper extremities more affected than lower
    • Clinical features
      • Spastic weakness of upper extremities
      • Less severe weakness of (or normal) lower extremities
      • Dissociated sensory loss affecting the distribution of the adjacent dermatomes
        • Loss of spinothalamic modalities: pain, temperature, crude touch
        • Preservation of dorsal column modalities: light touch, vibration, proprioception
      • Urinary dysfunction may occur
  • Posterior cord syndrome
    • = injury to posterior region of spinal cord
    • Etiology
      • Cervical spondylosis
      • Multiple sclerosis
      • B12 deficiency (subacute combined degeneration)
      • Tabes dorsalis (syphilis)
    • Pathomechanism
      • Injury to posterior part of spinal cord injures dorsal column -> dissociated sensory loss
    • Clinical features
      • Dissociated sensory loss below the level of the lesion
        • Loss of dorsal column modalities: crude touch, vibration, proprioception
        • Preservation of spinothalamic modalities, pain, temperature, light touch
      • Spastic muscle weakness below the level of the lesion
      • Sensory gait ataxia
  • Anterior cord syndrome
    • = injury to anterior region of spinal cord
    • Etiology
      • Anterior spinal artery syndrome (ASAS)
        • Aortic surgery
        • Aortic dissection
      • Hyperflexion injury
    • Pathomechanism
      • Anterior 2/3 of spinal cord is affected
      • Spinothalamic tract is close to the anterior part of the spinal cord, so injury to this region could damage spinothalamic tract (but preserve dorsal column) -> dissociated sensory loss
    • Clinical features
      • Dissociated sensory loss below the level of the lesion
        • Loss of spinothalamic modalities: pain, temperature, crude touch
        • Preservation of dorsal column modalities: light touch, vibration, proprioception
      • Initially flaccid weakness, later spastic weakness

43. Conus and cauda syndrome

  • Both syndromes are surgical emergencies
  • Conus medullaris syndrome
    • Etiology
      • Disc herniation
      • Trauma
    • Pathomechanism
      • Conus medullaris is the termination of the spinal cord, usually at the level of L1
    • Clinical features
      • Sudden onset
      • Bilateral and symmetric symptoms
      • Less severe pain
        • Pain radiates to the legs
      • Sensory symptoms
        • Perianal or saddle anaesthesia
        • Dissociated sensory loss
          • Impaired spinothalamic tract, intact dorsal column
      • Vegetative symptoms
        • Early onset of vegetative symptoms
        • Bladder incontinence
        • Faecal incontinence
        • Impotence
      • Motor symptoms
        • Weakness of lower extremities may be present
        • Fasciculations of lower extremity muscles
        • Achilles reflex absent but patellar reflex normal
  • Cauda equina syndrome
    • Etiology
      • Disc herniation
      • Trauma
    • Pathomechanism
      • Cauda equina is a bundle of nerve roots which continue down from the conus medullaris
      • Cauda equina syndrome occurs when some of the nerve roots are compressed
    • Clinical features
      • Gradual onset
      • Bilateral but asymmetric symptoms
      • More severe pain
        • Pain radiates to the legs
      • Sensory symptoms
        • Saddle anaesthesia
        • Sensory loss in the distribution of the affected nerve roots
        • No dissociated sensory loss
      • Vegetative symptoms
        • Late onset of vegetative symptoms
        • Bladder incontinence
        • Faecal incontinence
        • Impotence
      • Motor symptoms
        • Weakness of lower extremities may be present
        • Both Achilles and patellar reflex are absent

44. Clinical signs of plexus lesions

  • Brachial plexus lesions
    • = C5 – Th1
    • Etiology
      • Shoulder injury
      • Compression
    • Erb-Duchenne palsy
      • Upper brachial plexus lesion (C5 – C6)
      • Most common type
      • Motor symptoms
        • Paresis of deltoid, biceps, and forearm muscles
      • Sensory symptoms
        • Sensory loss of radial side of upper arm and shoulder
      • Reflexes
        • Absent biceps and radial reflexes
    • Dejerine-Klumpke palsy
      • Lower brachial plexus lesion (C8 – Th1)
      • Motor symptoms
        • Paresis of wrist and finger flexors
        • Paresis of small muscles of hand
      • Sensory symptoms
        • Sensory loss of ulnar half of hand and forearm
      • Associated with Horner syndrome
  • Lumbar plexus lesions
    • = Th12 – L4
    • Etiology
      • Trauma
    • Clinical features
      • Motor symptoms
        • Paresis of hip flexors and knee extensors
      • Sensory symptoms
        • Sensory loss of outer surface of thigh
  • Cervical plexus lesions
    • = C1 – C4
    • Rare
    • Etiology
      • Shoulder injury
      • Compression
    • Clinical features
      • ?
  • Sacral plexus lesions
    • = L4 – S4
    • Rare
    • Clinical features
      • ?

45. Signs of cervicobrachial radicular lesions

  • C5 root lesion
    • Sensory symptoms
      • Radial part of upper arm
    • Motor symptoms
      • Deltoid
      • Biceps
    • Reflex lost
      • Biceps reflex
  • C6 root lesion
    • Sensory symptoms
      • Radial part of upper and lower arm
      • Thumb and lateral half of index finger
    • Motor symptoms
      • Brachioradialis
      • Biceps
    • Reflex lost
      • Biceps reflex
  • C7 root lesion
    • Sensory symptoms
      • Middle finger, and the two adjacent halves of the second and fourth fingers
    • Motor symptoms
      • Triceps
      • Wrist pronator
    • Reflex lost
      • Triceps reflex
  • C8 root lesion
    • Sensory symptoms
      • Ulnar part of lower arm
      • Little finger and medial half of ring finger
    • Motor symptoms
      • Muscles of hand
    • Reflex lost
      • Triceps reflex

46. Signs of lumbosacral radicular lesions

  • L4 root lesion
    • Sensory symptoms
      • Outer side of thigh
      • Inner side of calf and ankle
    • Motor symptoms
      • Quadriceps
      • Tibialis anterior
    • Reflex lost
      • Patellar reflex
  • L5 root lesion
    • Sensory symptoms
      • Lateral side of knee
      • Anterior part of shin
      • First two toes
    • Motor symptoms
      • Extensor hallucis longus
    • Reflex lost
      • None important (only tibialis posterior reflex)
  • S1 root lesion
    • Sensory symptoms
      • Back part of thigh
      • Outer side of calf and ankle
      • Third, fourth, fifth toes
    • Motor symptoms
      • Peroneal muscles
      • Triceps surae
    • Reflex lost
      • Achilles reflex

47. Signs of ulnar nerve lesion, typical tunnel syndrome

  • See topic 49

48. Signs of medial nerve lesion, typical tunnel syndrome

  • Median nerve lesion
    • Sensory symptoms
      • Middle of the palm
      • Palmar aspect of first, second, and third fingers
      • Lateral half of the fourth finger
    • Motor symptoms
      • Thumb opposition
      • Thumb flexion
      • Thumb abduction
      • Flexion of third and fourth fingers
      • Thenar atrophy
  • Carpal tunnel syndrome
    • Most common cause of median nerve lesion
    • Etiology
      • Obesity
      • Female > male
      • Diabetes
      • Pregnancy
      • Certain repetitive wrist movements at work
    • Diagnosis
      • Carpal tunnel is a clinical diagnosis
      • Tinel sign
        • Applying pressure to the palmar side of the wrist causes paraesthesia in the area of the median nerve
      • Nerve conduction studies or electromyography can help the diagnosis
    • Treatment
      • Splinting
      • Glucocorticoid injection
      • Surgical decompression

49. Signs of ulnar nerve lesion, typical tunnel syndrome

  • Ulnar nerve lesion
    • Etiology
      • Cubital tunnel syndrome
      • Guyon canal syndrome
    • Sensory symptoms
      • On palmar palm: whole 5th finger + ulnar half of the 4th
      • On dorsal palm: whole 5th and 4th fingers + ulnar half of 3rd
    • Motor symptoms
      • Thumb adduction
      • Fourth finger flexion
      • Fifth finger flexion
      • Claw hand deformity
      • Atrophy of hypothenar and interosseous muscles
    • Froment sign
      • Procedure
        • Ask patient to hold a piece of paper between their thumb and index finger
        • Try to pull the paper out of their hands
      • Negative
        • Patient can hold the paper without difficulty
      • Positive
        • Patient flexes the thumb at the interphalangeal joint to compensate for the weakness of adductor pollicis brevis
          • The flexor pollicis longus is innervated by the median nerve
  • Cubital (elbow) tunnel syndrome
    • In the cubital tunnel of the elbow
    • Etiology
      • Repeated leaning on the elbow
      • Prolonged elbow flexion
      • Diabetes

50. Signs of radial nerve lesion, typical tunnel syndrome

  • Radial nerve lesion
    • Etiology
      • Fracture of humerus
      • Long-term compression
        • Falling asleep with one arm over furniture
    • Sensory symptoms
      • Radial half of the dorsal surface of the hand
    • Motor symptoms
      • Finger extensors
      • Wrist extensors
      • “Drop” hand
      • Atrophy of finger extensors
  • Radial tunnel syndrome (= Saturday night palsy)
    • Rare
    • Causes pain and weakness of wrist extensors
    • No sensory symptoms

51. Signs of peroneal nerve lesion, typical tunnel syndrome

  • (Common) Peroneal nerve lesion
    • (Also called common fibular nerve)
    • Etiology
      • Fracture of fibular head
      • Dislocation of knee
    • Sensory symptoms
      • Area between second and third toes
    • Motor symptoms
      • Tibialis anterior muscle (dorsiflexion)
      • Toe extensors
      • Atrophy of tibialis anterior
      • Foot drop -> steppage gait (topic 34)

52. Common signs of polyneuropathy

  • Polyneuropathy = generalized process affecting many peripheral nerves
  • Typical clinical features
    • Affects distal nerves
    • Affects lower limbs more often than upper
      • Typical “stocking and glove” distribution, with distal lower limbs and distal upper limbs affected
    • Symmetric distal anaesthesia, paraesthesia, or weakness
    • Pain may be present
    • Vibrational sense lost first
    • Urinary and faecal function normal

53. Signs of temporal lobe lesion

  • Wernicke aphasia
  • Temporal lobe epilepsy
  • Disturbance of hearing

54. Signs of frontal lobe lesion

  • Personality changes
    • Disinhibition
    • Aggression
  • Gegenhalten (paratonia)
    • Patient involuntarily resists movement, similar to rigidity
    • Unlike rigidity, gegenhalten becomes less prominent when patient is distracted
  • Broca aphasia (see topic 36)
  • Apraxic gait (see topic 34)
  • Frontal release signs
    • = return of primitive (infantile) reflexes in adulthood
      • Due to lesion of the inhibitory neurons in the frontal lobe
    • Grasp reflex
      • Touching the palm elicits grasping
    • Rooting reflex
      • Touching the corner of the mouth elicits movement of it
  • Contralateral upper motor neuron lesion with muscle weakness
  • Urinary incontinence
  • Ipsilateral conjugate deviation of the eyes
  • Akinetic mutism

55. Signs of parietal lobe lesion

  • Hemineglect
  • Homonymous lower quadrantanopia (see topic 27)
  • Apraxia (see topic 35)
  • Contralateral sensory loss
  • Gerstmann syndrome
    • Inability to recognize left and right
    • Agraphia
    • Acalculia

56. Signs of occipital lobe lesion

  • Homonymous hemianopia
  • Cortical blindness
  • Visual hallucination

57. Examination of alertness. Types of unconsciousness

  • Examination of alertness
    • Determine if patient is oriented to person, place, and time
    • Ask patient to name the months in order and backwards
    • Determine arousability in response to external stimuli (see topic 59)
  • Types of unconsciousness (disorders of vigilance/alertness)
    • In order from least to most unconscious:
    • Torpidity
      • Patient is alert but slowed down
    • Somnolence
      • Patient is superficially sleeping but can be awakened easily by sensory stimuli or verbal stimuli
    • Sopor
      • Patient can only be awakened by stronger stimuli
    • Stupor
      • Patient can only be awakened by strong pain
    • Coma
      • Patient cannot be awakened at all

58. Signs of raised intracranial pressure, types of intracranial herniations

  • Signs of increased ICP
    • Cushing triad/reflex
      • Hypertension
      • Bradycardia
      • Irregular respiration
    • Reduced level of consciousness
    • Headache
    • Vomiting
    • Papilloedema
    • Abducent palsy -> diplopia
  • Types of intracranial herniation
    • Subfalcine (cingulate) herniation
      • Cingulate gyrus herniates under falx cerebri
      • Clinical features
        • Compression of anterior cerebral arteries -> stroke
        • Can progress to other types of herniation
    • Uncal transtentorial herniation
      • Uncus herniates at tentorial incisure
      • Often caused by a unilateral mass effect
        • Haemorrhage
        • Infarct (-> swelling)
      • Clinical features
        • Impaired consciousness
        • Ipsilateral CN III palsy
          • Fixed, dilated pupil (Hutchinson’s pupil)
          • Later, downward and outer deviation of eye occurs
        • Contralateral motor deficit
        • Ipsilateral motor deficit (Kernohan’s sign)
          • Due to compression of the contralateral cerebral peduncle
          • One of the rare cases where a cortical lesion causes ipsilateral motor signs
    • Central transtentorial herniation
      • Hemispheres, basal ganglia and diencephalon herniate through tentorial notch into the midbrain
      • Often caused by diffuse or bilateral mass effect
        • Diffuse or multifocal swelling
        • Bilateral haematomas
      • Clinical features
        • Impaired consciousness
        • Compression of the vein of Galen
          • Venous congestion
          • Cerebral oedema
        • Compression of cerebral aqueduct -> obstructive hydrocephalus
        • Stretching of the basilar artery -> potential rupture
    • Foramen magnum (tonsillar) herniation
      • Cerebral tonsils herniate through foramen magnum
      • Clinical features
        • Compression of brainstem
          • -> Impaired consciousness
          • -> Impaired circulation
          • -> Impaired respiration -> apnoea

59. The Glasgow coma scale (GCS) and assessment

  • Glasgow coma scale
    • Is used to assess neurological status, trauma severity, and prognosis in patients with traumatic brain injury
      • Also used in subarachnoid haemorrhage, bacterial meningitis, encephalitis, and other neurological diseases
    • GCS gives total score between 3 and 15, where 15 is best
    • Three parameters are evaluated: best eye response, best verbal response, and best motor response in response to various stimuli
    • Should be tested before intubation
    • Result
      • The individual parameters should also be recorded!
        • E.g. GCS 9 = E2 V4 M3
      • GCS score 13 – 15 = mild brain injury
      • GCS score 9 – 12 = moderate brain injury
      • GCS score 3 – 8 = severe brain injury
        • Intubation is indicated

Eye opening

Verbal response Motor response Points
Obeys commands

6

Oriented Localized response to pain (movement toward painful stimulus) 5
Spontaneously Confused Withdrawal response to pain

4

To verbal command

Inappropriate words Decorticate posture in response to pain 3
To pain Incomprehensible sounds Decerebrate posture in response to pain

2

No eye opening

No verbal response No motor response

1

“C” Theoretical questions from lectures

(Ischaemic stroke)

  • 80% of strokes
  • Subtypes
    • Large artery occlusion
      • 20 – 25% of ischaemic strokes
      • Due to occlusion of large arteries
        • Middle cerebral artery > internal carotid > vertebral, ACA, etc
        • Often due to atherosclerotic rupture
      • Worst subtype
      • Causes large infarct (> 1,5 cm diameter)
      • Can affect both cortex and subcortical regions
    • Small artery occlusion/lacunar stroke
      • 25% of ischaemic strokes
      • Due to occlusion of penetrating small arteries
        • Also called lenticulostriate arteries
        • These are small arteries which arise at acute angles from large cerebral arteries
        • Chronic hypertension causes lipohyalinosis of these arteries, causing occlusion
      • Causes small infarct (< 1,5 cm diameter)
      • Mostly affect subcortical regions (basal ganglia, brainstem)
      • Clinical features
        • No cortical symptoms
        • Pure hemiparesis
        • Pure hemisensory loss
        • Ataxic hemiparesis
        • Dysarthria-clumsy hand syndrome
    • Cardioembolic stroke
      • 20% of ischaemic strokes
      • Arterial occlusion presumably due to embolus from heart
      • A cardiac source of embolus must be identified
        • AF, MI, endocarditis, etc.
    • Cryptogenic stroke
      • 25 – 30% of ischaemic stroke
      • Ischaemic stroke in which the etiology can not initially be determined
      • Most commonly due to
        • Paroxysmal AF
        • PFO with paradoxical embolism
        • Non-atherosclerotic vasculopathy

(Haemorrhagic stroke)

  • Intracerebral haemorrhage (ICH)
    • 10 – 15% of all strokes
    • Etiology
      • Hypertension
      • Vascular malformation (more common in younger patients)
      • Cerebral amyloid angiopathy
    • Pathology
      • Hypertension -> haemorrhage in subcortical regions (putamen, thalamus, etc.)
      • Vascular malformation -> lobar haemorrhage
  • Subarachnoid haemorrhage (SAH)
    • 6 – 10% of all strokes
    • Etiology
      • Rupture of intracranial aneurysm
      • Arteriovenous malformation
    • Pathology
      • Congenital malformation of tunica media + hypertension -> intracranial aneurysm
      • Acute hypertension may rupture aneurysm

(Transient ischaemic attack)

  • Definition
    • Old definition: full resolution of symptoms within 24 hours
    • New definition: transient neurological dysfunction caused by ischaemia without infarction
      • New definition requires MRI with DWI sequence for diagnosis
  • Clinical features
    • Similar to those of ischaemic stroke (see topic 60)
    • Most symptoms resolve within 1 hour
    • Most patients present after symptoms have resolved
    • Most often acute
  • Differential diagnosis
    • Migraine with aura
    • Todd’s paralysis (post-seizure neurologic deficit)
    • Hypoglycaemia
    • Intracranial structural lesions (tumour, haemorrhage, etc.)
    • Syncope
    • BPPV, labyrinthitis, Meniere disease
    • Brain abscess, encephalitis
    • Demyelinating disorders (multiple sclerosis)

(Malignant middle cerebral artery infarction)

  • Epidemiology
    • < 10% of ischaemic strokes
    • More common in younger patients (< 60 years)
  • Pathomechanism
    • Due to occlusion of middle cerebral artery or internal carotid
    • Causes cerebral oedema of whole hemisphere -> transtentorial herniation
    • Rapid worsening of symptoms over days
  • Prognosis
    • Up to 80% mortality
  • Treatment
    • Hemicraniectomy (see topic 62)

60. Symptoms of acute stroke

  • Symptoms of ischaemic stroke
    • See topics 23, 24
  • Symptoms of haemorrhagic stroke
    • Symptoms of subarachnoid stroke
      • Symptoms appear suddenly
      • Thunderclap headache
        • Sudden, severe headache (characteristically described as the worst headache the patient has experienced)
        • Occurs in 97% of cases
      • Meningism
        • Stiff neck
        • Photophobia
        • Nausea, vomiting
      • Impaired consciousness
      • Focal neurological signs
        • See topics 23, 24
      • Cranial nerve palsy
      • Seizure
    • Symptoms of intracerebral stroke
      • Symptoms progress gradually (over minutes or hours)
      • Headache
      • Focal neurological signs
        • See topics 23, 24
      • Signs of increased ICP (see topic 58)

61. Diagnostic steps in acute stroke

  • Ensuring medical stability (airways, breathing, circulation)
  • ECG
  • Labs
    • CBC
    • INR
    • Glucose
    • Electrolytes
  • Diagnostic imaging
    • Purpose
      • To exclude haemorrhage as a cause of stroke
        • If patient has clinical symptoms of stroke and no haemorrhage on imaging, they have ischaemic stroke until proven otherwise
    • ECG and labs should not delay diagnostic imaging!
    • Non-contrast CT (first choice)
      • Can not detect ischaemia in the first 6 hours
      • Can sometimes detect hyperdense vessels, a sign of a clot in the vessel
    • MRI with DWI sequence (alternative)
      • Is superior to non-contrast CT but is less available and more often contraindicated
      • Can detect ischaemia after 30 minutes
  • Vascular imaging
    • After initial diagnostic imaging
    • Purpose
      • To detect occlusion of large artery
        • If present, patient may be eligible for mechanical thrombectomy
      • To evaluate collateral circulation
        • Good collateral -> better outcome of revascularization therapy
      • To evaluate whether there is atherosclerosis present, which would suggest a thrombotic etiology
    • Modalities
      • Carotid ultrasound
      • CT or MRI angiography
  • Perfusion imaging
    • Indicated if the findings may influence the decision to perform thrombectomy after the initial 6 hour window
    • Can be performed simultaneously with vascular imaging
    • Purpose
      • To determine the size of the penumbra, the brain volume which is potentially salvageable by revascularization
    • Modalities
      • MRI with DWI and PWI
      • CT perfusion
  • Cardiological investigation
    • Done if a cardiac etiology of stroke is suspected, or there is cryptogenic stroke
    • Modalities
      • Transthoracic echocardiography
        • Can not detect PFO
      • Transoesophageal echocardiography
        • Can detect PFO
      • Holter ECG
        • Normal ECG at admission does not exclude paroxysmal AF
        • Sensitivity of Holter to detect paroxysmal AF increases with the duration of the ECG monitoring

62. Management of acute stroke

  • Management of acute ischaemic stroke
    • Admission to stroke unit
    • IV thrombolysis
      • With a rtPA (recombinant tissue plasminogen activator)
        • Alteplase, duteplase, tenecteplase
      • Can be used for both large artery and small artery occlusion
        • But it is less effective for large artery occlusion, therefore it should be combined with thrombectomy
      • Time window: Within 4,5 hours of symptom onset
        • The sooner, the better
      • Risk
        • Relatively safe
        • May increase risk of haemorrhage
        • Haemorrhage as cause of stroke must be ruled out first
      • Contraindications
        • INR > 1,7
    • Mechanical thrombectomy
      • If there is large artery occlusion
        • Large artery means internal carotid, basilar, vertebral arteries, or large segments of middle or anterior cerebral artery
        • 10% of ischaemic stroke are due to large artery occlusion
        • Thrombolysis has poor effect on large artery occlusion
      • Time window: Within 6 hours of symptom onset
        • Can be extended to up to 24 hours if there is a large penumbra (salvageable brain area)
        • MRI with perfusion sequencing necessary to determine the size of the penumbra
      • Should be combined with thrombolysis if within the 4,5 hour time window
    • Aspirin
      • For all cases of acute ischaemic stroke
      • Given within 48 hours of symptom onset and continued indefinitely
      • In patients given thrombolysis aspirin should be delayed until after the 24 hour post-thrombolysis imaging has excluded haemorrhage
      • Aspirin decreases recurrence rate
    • Decompressive hemicraniectomy
      • If there is malignant MCA infarction (see below)
      • Within 48 hours of symptom onset
      • Reduces mortality substantially, but has high risk of disability
    • Blood pressure management
      • Blood pressure during stroke is usually high
      • Purpose
        • Decrease blood pressure
        • But don’t treat too aggressively! Avoid too low blood pressure
      • If patient does not receive thrombolytics
        • Target BP < 220/120 mmHg
      • If patient does receive thrombolytics
        • Target BP < 185/110 mmHg
      • Drugs
        • Labetalol
        • Enalapril
        • Nitroprusside
        • Nitropaste
    • Blood glucose management
      • Insulin titration if serum glucose > 10 mM
    • Fluid replacement therapy
      • Patients with stroke are often fluid deprived
      • Isotonic saline is recommended if needed
  • Management of acute haemorrhagic stroke
    • Admission to stroke unit
    • Reverse anticoagulation (if patient was on it)
    • Blood pressure management
      • Systolic target BP varies from 140 to 160 mmHg
        • Depending on type of haemorrhage and original BP
    • Blood glucose management
      • Insulin titration if serum glucose > 10 mM
    • Surgical evacuation of haemorrhage
      • On certain indications
        • Large cerebellar haemorrhage
        • Brainstem compression
        • Hydrocephalus
    • Prevent vasospasm
      • With nimodipine
      • For SAH
    • Aneurysm repair
      • For aneurysmal SAH
      • Methods
        • Surgical clipping
        • Endovascular coiling

63. Diagnostic test in case of TIA, clinical significance

  • Diagnostic steps in case of TIA
    • Ensuring medical stability (airways, breathing, circulation)
      • Rarely necessary for TIA
    • ECG
    • Labs
      • CBC
      • INR
      • Glucose
      • Electrolytes
    • Diagnostic imaging
      • Purpose
        • To exclude haemorrhage
        • To show that there is no infarction, thereby differentiating TIA from stroke
      • ECG and labs should not delay diagnostic imaging!
      • MRI with DWI sequence (first choice)
        • Can differentiate between ischaemia and infarct very early
      • Non-contrast CT (second choice)
        • Can not detect ischaemia in the first 6 hours
    • Vascular imaging
      • After initial diagnostic imaging
      • Purpose
        • To detect occlusion of large artery
          • If present, patient may be eligible for mechanical thrombectomy
        • To evaluate collateral circulation
          • Good collateral -> better outcome of revascularization therapy
        • To evaluate whether there is atherosclerosis present, which would suggest a thrombotic etiology
      • Modalities
        • Carotid ultrasound
        • CT or MRI angiography
    • Cardiological investigation
      • Done in all cases
      • Modalities
        • Transthoracic echocardiography
        • Transoesophageal echocardiography
        • Holter ECG
          • Normal ECG at admission does not exclude paroxysmal AF
          • Sensitivity of Holter to detect paroxysmal AF increases with the duration of the ECG monitoring
    • ABCD2 score
      • To determine risk of later stroke
      • The higher the score, the higher the risk
      • 1 or 2 points for each feature present
      • Depends on
        • A – Age > 60
        • B – Blood pressure > 140/90 mmHg
        • C – Clinical features
          • Hemiparesis or aphasia
        • D – Duration > 60 minutes
        • D – Diabetes
      • If the score is high, the patient should be treated as in-patient
  • Clinical significance of TIA
    • By definition TIA does not cause permanent neurological dysfunction
    • However, TIA is a major risk factor for ischaemic stroke
      • Highest risk in the first days after TIA
      • 20% risk for stroke 3 months after TIA
    • A patient with TIA should receive secondary prevention of stroke similar to a person who had stroke (see topic 64)

64. Secondary prevention of stroke

  • Secondary prevention of ischaemic stroke
    • Antiplatelet therapy
      • For patient with established atherosclerosis
      • Aspirin or P2Y12 antagonist (clopidogrel, etc.)
      • Start within 48 hours of ischaemic stroke onset and continue indefinitely
        • Should not be started for 24 hours after thrombolysis
    • Cholesterol management
      • For all patients who had ischaemic stroke
        • Statin therapy is beneficial even for patients without high LDL
      • Statins
      • Target LDL < 1,4 mM or at least 50% reduction from baseline
    • Blood pressure management
      • For patients with hypertension without diabetes, the target is < 140/90 mmHg
      • For patients with hypertension and diabetes, the target is < 120/80 mmHg
    • Blood glucose management
      • For patients with diabetes
      • Target HbA1c < 7% (53 mmol/mol)
    • Anticoagulation
      • For patients with atrial fibrillation
      • NOAC is preferred over VKA
    • Carotid surgery
      • Indicated in patients with 70 – 99% carotid stenosis
      • As soon as possible after ischaemic event
      • Carotid endarterectomy or carotid artery stenting
  • Secondary prevention of haemorrhagic stroke
    • Blood pressure management
      • Specific target depends on presence of other risk factors, etc.

65. Differential diagnostics of unconsciousness

  • See topic 17, 18

66. Convulsive syncope

  • = Form of syncope which is accompanied by myoclonic jerks and tonic stretching
  • Etiology
    • Vasovagal syncope
    • Cardiogenic syncope
      • Arrhythmia
      • Myocardial infarction
      • Pulmonary embolism
    • Hypoglycaemia
    • Antihypertensive drugs
  • Pathomechanism
    • > 10 second globally decreased CBF
  • Clinical features
    • Usually brief (< 20 seconds)
    • Myoclonic jerk
    • Tonic stretching
    • Tongue bite on the apex of the tongue
    • Enuresis
    • Eyes remain open
  • Must be differentiated from true seizure

67. Grand mal seizure

  • = tonic-clonic seizure
  • Epidemiology
    • Most common type of seizure
  • Etiology
    • Epilepsy
    • Electrolyte disturbances
    • Brain tumour
    • Alcohol withdrawal
    • Traumatic brain injury
    • Hypoglycaemia
    • Stroke
    • CNS infection
    • Fever (in children)
  • Clinical features
    • Ictal phase (during seizure)
      • Lasts 30 seconds – 2 minutes
      • Tonic phase
        • Lasts 10 – 20 seconds
        • Sudden loss of consciousness
          • Person drops to the floor
        • Extension of back, neck, arms, legs
        • Ictal “cry” (sound due to contraction of laryngeal muscles)
        • Rotated eyes
        • Apnoea or shallow respiration
        • Pale or cyanosis
      • Clonic phase, with clonus
        • Lasts 30 – 90 seconds
        • Generalized flexor contractions alternating with progressively longer muscle relaxation
        • Biting the lateral aspect of the tongue
        • Cyanosis
        • Foaming at the mouth
        • Bladder or bowel incontinence
    • Postictal phase (after seizure)
      • Can last anywhere from a few minutes to an hour
      • Todd paresis (transient hemiparesis)
      • Unresponsiveness
      • Confusion
      • Amnesia
      • Fatigue
      • Myalgia
      • Aphasia
  • Diagnosis
    • Determine whether it was a true seizure or syncope, pseudoseizure, etc.
    • Determine whether it was a symptomatic seizure (due to underlying disease) or unprovoked
    • ECG
    • EEG
    • CT/MRI
      • To look for structural lesions in brain
    • Labs
  • Treatment
    • No treatment for the seizure itself (unless it develops into status epilepticus)
    • Treatment of the underlying condition, or treatment of the epileptic syndrome

68. Status epilepticus, definition, and management

  • Definition:
    • Any of the three:
    • A single seizure lasting longer than 5 minutes
    • More than one seizure without recovery of consciousness in-between
    • More than two grand mal seizures within 4 hours
  • Clinical significance
    • Life-threatening!
    • 20% mortality
    • May cause cerebral oedema, aspiration, cardiovascular failure, rhabdomyolysis, hyperthermia, etc.
  • Treatment
    • Ensure stability (ABC)
    • 1 ampulla IV lorazepam or other BZD
      • Alternative if no IV access: IM or buccal or rectal midazolam
      • If no response within 1 minute -> give another dose
    • If no resolution after 5 minutes: IV valproate, levetiracetam, or fosphenytoin
      • (According to UpToDate we give this simultaneously as BZD)
      • According to our teacher you only give it if BZD doesn’t resolve after 5 minutes
    • Look for cause
      • Electrolytes, glucose, inflammatory markers, etc.
  • Refractory status epilepticus
    • = status epilepticus which does not stop after BZD + non-BZD antiepileptic for 40 minutes
    • Treatment: Continuous infusion of midazolam or propofol

69. Differential diagnostics of vertigo

  • Differential diagnosis is mostly based on history and clinical features
  • Differential diagnosis of central vertigo
Disorder Duration of episode Recurrence of vertigo Other symptoms Other clinical features
Vestibular migraine Minutes Recurrent episodes Headache, other symptoms of migraine None
TIA of vertebrobasilar system Minutes Single or multiple episodes Other brainstem or cerebellar symptoms MRI confirms ischaemia
Brainstem stroke Days Single episode Other brainstem symptoms MRI confirms infarct
Cerebellar stroke Days Single episode Other cerebellar symptoms MRI confirms infarct
  • Differential diagnosis of peripheral vertigo
Disorder Duration of episode Recurrence of vertigo Other symptoms Other clinical features
Benign paroxysmal positional vertigo Seconds Recurrent episodes Specific head movements and positions precipitate symptoms Positive Dix-Hallpike test
Ménière disease Hours Recurrent episodes Hearing loss, tinnitus Audiometry shows SN hearing loss
Vestibular neuritis Days Single episode Symptoms of viral infection earlier or during None
Otitis media Days Single episode Ear pain Characteristic findings on otoscopy

70. The common features of peripheral vertigo

  • See topic 30

71. The common features of central vertigo

  • See topic 30

(Parkinson disease)

  • Idiopathic cause of parkinsonism
  • Clinical features
    • Unilateral onset
    • Slow progression
    • Parkinsonism
      • Bradykinesia in addition to resting tremor or rigidity
    • “Pill-rolling” rest tremor
    • Expressionless face
    • Hypokinetic gait
    • Small handwriting

72. Diagnostics and differential diagnostics of Parkinson’s disease

  • Diagnosis of Parkinson disease (PD)
    • In typical presentations, only anamnesis and physical examination are necessary
    • In less typical presentations an MRI or MIBG scintigraphy can be used to exclude many other causes of parkinsonism
    • Parkinson disease is a clinical diagnosis based on the MDS diagnostic criteria
    • A definitive diagnosis requires:
      • Diagnosis of parkinsonism
      • Two supportive criteria
      • No absolute exclusion criteria
      • No red flags
    • A probable diagnosis requires:
      • Presence of bradykinesia plus resting tremor or rigidity
      • No absolute exclusion criteria
      • Presence of red flags counterbalanced by supportive criteria
    • Supportive criteria
      • Beneficial response to dopaminergic therapy
      • Presence of levodopa-induced dyskinesia
      • Resting tremor
      • Olfactory loss
      • Cardiac sympathetic denervation on MIBG scintigraphy
    • Absolute exclusion criteria
      • Cerebellar symptoms
      • Concomitant anti-dopamine drug therapy
      • Cortical sensory loss
      • Diagnosis of another condition known to cause parkinsonism
      • +++
    • Red flags
      • Rapid progression of gait impairment
      • Absence of progression of motor symptoms
      • Severe dysphonia, dysarthria, or dysphagia
      • +++
  • Differential diagnosis of parkinsonism
    • Parkinson disease
    • Secondary parkinsonism
      • Drug-induced
        • Antipsychotics
        • Antiemetics
        • +++
      • Metabolic
        • Wilson disease
        • Chronic liver failure
        • +++
      • Infections
        • HIV
        • Encephalitis lethargica
      • Structural brain lesions
        • Hydrocephalus
        • Tumour
        • Chronic subdural haematoma
        • +++
      • Trauma
      • Cerebrovascular disease
      • Toxins
    • Parkinson-plus syndromes
      • Types
        • Dementia with Lewy-bodies
        • Multiple system atrophy
        • Corticobasal degeneration
        • Progressive supranuclear palsy
      • Differentiating features
        • Poor response to dopaminergic therapy
        • Faster progression than PD
        • Presence of other neurological symptoms
          • Dementia
          • Oculomotor palsy
          • Autonomic dysfunction
          • Gait instability
      • Diagnosis
        • By imaging

73. Treatment of Parkinson’s disease

  • Choice of therapy depends on age and symptom severity
    • In mild cases treatment may not be necessary
  • Non-medical therapy
    • Physiotherapy
    • Speech therapy
  • Levodopa + carbidopa/benserazide
    • Most potent antiparkinsonian drug
    • Has effect in virtually all patients with PD
      • If the patient experiences no effect, they most likely have don’t have PD
    • Preferred in patients with moderate or severe symptoms at any age
    • The lowest dose which gives adequate benefit should be used
      • Rather than using a higher dose to eradicate all symptoms
    • Patients initially have very good effect, the so-called “honeymoon period”, with no motor fluctuations or dyskinesias
    • The patient experiences dyskinesias and motor fluctuations more and more often over time
      • It was previously believed that levodopa increases the rate of progression of PD, and so it should be started as late as possible to “ration” its effects
      • Nowadays we’re pretty sure that that’s not true. Instead, we now know that it is the natural progression of PD which reduces the effect of levodopa, and not the levodopa treatment itself
        • As the PD progresses and the brain’s dopamine production decreases, the fluctuations in plasma levels of levodopa cause larger and larger fluctuations in brain dopamine levels
      • So, the choice and timing of initial therapy does not impact the long-term incidence of dyskinesia and motor fluctuations, and there’s no reason not to start levodopa early
      • When the patient begins to experience these late side effects, a specialist should re-evaluate dosage, dosing schedules, choice of drugs, etc., in order to reduce them
    • Levodopa exists in immediate release (normal) and controlled release formulations
      • Controlled release formulations may decrease the incidence of dyskinesias and motor fluctuations
    • Side effects
      • Nausea
      • Somnolence
      • Headache
      • Psychiatric symptoms
        • Hallucination
        • Agitation
        • Psychosis
      • Dyskinesia
        • Usually occurs 30 – 90 minutes after taking a dose, as the action of the drug peaks (so-called “peak dose dyskinesia”)
      • Motor fluctuations (= “on – off phenomenon”)
        • “Wearing off” = symptoms return as the dose of levodopa diminishes, 3 – 4 hours after a dose
        • “Unpredictable off” = symptoms return with no obvious relationship to the time of levodopa dosing
        • “Dose failure” or “no-on response” = a dose fails to improve symptoms
  • Dopamine agonists
    • Agents
      • Pramipexole
      • Ropinirole
      • (Bromocriptine is associated with fibrosis and so is rarely used)
    • Less effective than levodopa
    • More non-motor side effects but fewer motor side effects
      • Rarely cause dyskinesia or motor fluctuations
    • Withdrawal syndrome occurs in case of abrupt cessation
      • Anxiety
      • Panic attack
      • Nausea
      • Dizziness
  • Monoamine oxidase type B (MAO-B) inhibitors
    • Agents
      • Selegiline
      • Rasagiline
      • Safinamide
    • Low effectiveness
    • Generally well tolerated – few side effects
    • Good first choice in mild PD
  • Amantadine
    • Has antiviral, dopaminergic, anticholinergic, anti-NMDA, and amphetamine-like effects
    • Low effectiveness
      • Effect decreases over time
    • Good second choice in mild PD
    • Effective in reducing dyskinesia of levodopa treatment
    • Non-severe side effects
      • Leg oedema
      • Livedo reticularis
  • Catechol-O-methyl transferase (COMT) inhibitors
    • Agents
      • Entacapone
      • Opicapone
    • These drugs prolong effect of levodopa
    • Effective in reducing motor fluctuations of levodopa treatment
  • Anticholinergics
    • Agents
      • Trihexyphenidyl
      • Benztropine
    • Effective against tremor but not for other symptoms
    • Not used in older (> 65 years) patients due to increased side effects
    • Side effects
      • Dry mouth
      • Blurred vision
      • Constipation
      • Urinary retention
      • Impaired memory
      • Confusion
  • Apomorphine
    • A dopamine agonist
    • Used for “rescue therapy” for “off periods” in levodopa treatment
    • Given as subcutaneous injection
      • Onset within 15 minutes
    • May also be given as a continuous subcutaneous apomorphine infusion (CSAI) via a pump
  • Deep brain stimulation (DBS)
    • Most frequently performed surgical procedure for PD
    • Involves placing electrodes in the subthalamic nucleus or internal globus pallidus
    • Highly effective, but carries risk for surgical complications, equipment complications, and stimulation-related complications
    • Reserved for patients who have reduced quality of life despite optimal medical treatment
  • Levodopa-carbidopa intestinal gel (LCIG) infusion
    • Involves a percutaneous gastrojejunostomy tube which infuses a levodopa-carbidopa gel into the jejunum continuously
      • A pump gives a morning bolus followed by a continuous maintenance dose during the day
    • Usually used in patients who don’t want DBS
    • Complications
      • Polyneuropathy
      • Postoperative wound infection
      • Abdominal pain
  • Older surgical procedures
    • Pallidotomy, thalamotomy, subthalamotomy
    • Effective, but invasive and destructive
    • Rarely performed nowadays

74. The main types of dystonia and treatment

  • Dystonia = a movement disorder with sustained or intermittent muscle contractions causing abnormal movements or postures
  • Types according to age
    • Early-onset dystonia
      • Onset < 20 years
      • Usually generalized
    • Adult-onset dystonia
      • Onset > 20 years
      • Usually focal or segmental
  • Types according to cause
    • Primary dystonia
      • Idiopathic
      • Normal brain MRI
      • Dystonia is the only symptom
    • Secondary dystonia
      • Secondary to
        • Antipsychotic drugs
        • Huntington disease
        • Wilson disease
        • Stroke
      • Other neurological symptoms are present
  • Types according to affected site
    • Focal dystonia
      • Affects a single region
      • Most are idiopathic
    • Segmental dystonia
      • Affect multiple regions
    • Generalized dystonia
      • Affect the whole body or close to it
      • Usually early-onset
    • Hemidystonia
      • Affects one body side
  • Types according to clinical features
    • Mobile dystonia
      • Most dystonias are mobile
      • Symptoms are observable during movement
      • EMG shows burst activity
    • Fixed dystonia
      • Usually acute and affects young women
      • Symptoms are observable in rest
      • Skeletomuscular deformity is present
  • Specific dystonias
    • Cervical dystonia (= spasmodic torticollis)
      • A focal, primary dystonia
      • Sudden, painful contraction of sternocleidomastoid
    • Hand dystonia
      • A focal, primary dystonia
      • Non-painful contractions in the hand or arm, making it difficult to write or play instruments
      • Occurs in musicians or when writing
    • Eye dystonia (= blepharospasm)
      • A focal, primary dystonia
      • Spasm of periocular muscles, causing involuntary twitching or blinking
      • Can be isolated or part of Meige syndrome
    • Laryngeal dystonia
      • A focal, primary dystonia
      • Spasm of vocal cord muscles, causing voice breaks and strained voice
    • Oromandibular dystonia
      • A focal, primary dystonia
      • Spasm of muscles of mouth and jaw, causing chomping movements
      • Can be isolated or part of Meige syndrome
    • Meige syndrome
      • A segmental, primary dystonia
      • Presence of both blepharospasm and oromandibular dystonia
    • Early-onset isolated dystonia
      • Begins in childhood
      • Usually begins in the leg, eventually progressing to becoming generalized
    • Dopa-responsive dystonia
      • An early onset, generalized, primary dystonia
      • Typically presents in childhood
      • Symptoms worsen as the day wears on
      • Responds very well to levodopa treatment
    • Neuroleptic-induced dystonia
      • An adult onset, generalized, secondary dystonia
      • Especially affects face and neck
  • Treatment of dystonia
    • Levodopa
      • First-line treatment
      • May improve symptoms in all dystonias, but will also confirm or exclude the diagnosis of dopa-responsive dystonia
    • Botulinum toxin injection
      • For focal dystonias
    • Other pharmacological therapies
      • Anticholinergics
      • Baclofen
      • Benzodiazepines
    • Deep brain stimulation
      • If other treatments fail

75. Multiple sclerosis. Diagnostic steps and differential diagnostics

  • Epidemiology
    • Women > men
    • Age of onset 20 – 40 years
    • More common in whites
  • Pathomechanism
    • Idiopathic sites (plaques) of demyelination
    • Periventricular areas, spinal cord, brainstem, and cerebellum most commonly affected
  • Clinical course
    • Usually presents with an attack of neurological symptoms which last for days, but then improve over weeks
    • In the most common subtype (relapsing-remitting MS), the patient will experience more relapses in the future
    • Patients with relapsing-remitting MS may eventually develop secondary progressive MS, where there is a gradual increase in neurological symptoms with superimposed relapses
    • 10 – 20% present with primary progressive MS, where there is a gradual progression with no remission or relapse
  • Clinical features
    • Unilateral optic neuritis -> impaired vision
    • Internuclear ophthalmoplaegia
    • Cerebellar symptoms
    • Spinal cord symptoms
      • Absent superficial reflexes
      • Upper motor neuron lesion
      • Sensory loss
    • Fatigue
  • Diagnosis
    • Diagnosis is made when the patient fulfils the so-called McDonald criteria
      • These criteria require evidence of lesions in the CNS in different places and at different times (so-called “dissemination in space and time”)
      • Presence of oligoclonal bands in CSF can act as a substitute for dissemination in time
    • In some patients, the diagnosis can be made after a single attack
      • If they have evidence of dissemination in both space and time
    • Dissemination in space is evidenced when either of the following apply
      • Lesions on MRI in two MS-typical regions in the CNS
      • Clinical features which suggest lesions in multiple sites in the CNS
    • Dissemination in time is evidenced when either of the following apply
      • Presence of both gadolinium-enhancing and non-enhancing lesions on a gadolinium contrast MRI
        • Gadolinium-enhancing lesions are maximum a few weeks old, while non-enhancing lesions are older than that
      • Presence of a new gadolinium-enhancing lesion on a follow-up contrast MRI
      • Development of an additional clinical attack
    • Modalities used in diagnosis
      • MRI (with and without gadolinium contrast)
      • Lumbar puncture (shows oligoclonal bands in CSF)
      • Visually evoked potentials (VEP)
        • Shows slowed nerve conduction
        • Used if other tests are inconclusive
  • Differential diagnosis
    • Systemic lupus erythematosus
    • Sarcoidosis
    • Behcet disease
    • Neuroborreliosis
    • Neurosyphilis

76. Investigations in case of polyneuropathy

  • Anamnesis and physical examination
    • The time course (acute/subacute/chronic) is especially important
  • Labs
    • CBC, CRP, kidney function, liver function, TSH
    • Glucose
    • Serum protein electrophoresis
    • Autoantibodies
    • B12, folate
  • Nerve conduction studies (NCS) (= electroneurography (ENG))
    • Often performed
    • Can differentiate demyelination and axon loss
    • Can show the distribution of involvement
  • Electromyography (EMG)
    • Often performed
    • Can differentiate neurogenic and myopathic disease
    • Can show the distribution of involvement
  • Nerve biopsy
    • Rarely performed
    • If vasculitis is suspected
    • Sural or peroneal nerves are biopsied
  • Skin biopsy
    • Rarely performed
    • If polyneuropathy of small, unmyelinated nerve fibres is suspected

77. Specific types of polyneuropathies and their treatment

  • Diabetic neuropathy
    • Most commonly distal symmetric sensorimotor polyneuropathy
    • Other types
      • Autonomic neuropathy
      • Diabetic neuropathic cachexia/painful
      • Cranial neuropathy
      • Radiculoplexus neuropathy
    • Treatment
      • Some types spontaneously resolve
      • Tight blood glucose control
      • Neuropathic pain management
        • SNRI
        • Tricyclic antidepressants
        • Gabapentin/pregabalin
        • Capsaicin
  • Alcoholic polyneuropathy
    • Due to alcohol and thiamine deficiency
    • Treatment
      • Abstinence from alcohol
      • Thiamine supplementation
  • Guillain-Barré syndrome
    • Etiology
      • Upper respiratory tract or gastrointestinal infection 1 – 4 weeks earlier
    • Pathomechanism
      • Immune reaction against an earlier infection forms antibodies which target antigens on Schwann cells, causing demyelination
    • Clinical features
      • Symmetric flaccid muscle weakness which progresses over 1 – 4 weeks
        • Weakness usually begins in legs and ascend from there
        • Most patients peak at week 2
      • Absent deep tendon reflexes
      • Paraesthesia in hands and feet
      • 10 – 30% develop severe respiratory muscle weakness, requiring ventilatory support
      • Dysautonomia
        • Diarrhoea/constipation
        • Arrhythmia
    • Subtypes
      • Acute inflammatory demyelinating polyneuropathy (the most common type, described above)
      • Chronic inflammatory demyelinating polyneuropathy
      • Miller Fisher syndrome
    • Diagnosis
      • Based on diagnostic criteria
      • Features which must be present:
        • Progressive weakness of legs and arms
        • Decreased or absent reflexes
      • Features which support diagnosis
        • Progression of symptoms over 1 – 4 weeks
        • Symmetric symptoms
        • Mild sensory symptoms
        • Autonomic dysfunction
        • CSF shows albuminocytologic dissociation (= high protein but normal cell count)
        • Nerve conduction studies and EMG show demyelination
        • +++
    • Treatment
      • All patients should be admitted for monitoring
      • Intravenous immunoglobulin or plasma exchange
        • To all patients
        • Both are equally effective
      • Never give steroids!
  • Hereditary polyneuropathies
    • Hereditary motor sensory neuropathies (HMSN)
    • Hereditary sensory autonomic neuropathies (HSAN)
    • Distal hereditary motor neuropathies (dHMN)

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