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Shorties > Neuro > Flashcards

Neuro Flashcards

1
Q

Causes of CN I (Olfactory Nerve) Palsy

A

Causes of CN I palsy

  • Head injuries due to shearing of olfactory nerve filaments or fracture of the cribiform plate
  • Frontal lobe tumour or abscess
  • Ethmoid tumours
  • Meningiomas of olfactory groove
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2
Q

Finding in CN I (Olfactory Nerve) Palsy?

A

Anosmia

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3
Q

Explain the difference in findings between pre-chiasmic, chiasmic and post-chiasmic CN II (Optic N) lesions?

A

Pre-chiasmic: Unilateral blindness, unilaterally unreactive pupil (but the pupil would react with the consensual pupillary reaction)

Chiasmic: Bitemporal hemianopsia

Post-chiasmic: Homonymous hemianopia or quadrantanopia depending on location of the lesion

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4
Q

Causes of prechiasmic CN II lesions (CN II = Optic nerve)

A

of sphenoid bone (transecting the optic nerve)
Retinal tumors
Masses compressing the optic nerve

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5
Q

Causes of lesions at CN II chiasm (CN II = Optic nerve)

A

Pituitary adenoma
Craniopharyngioma
Saccular Berry aneurysm at optic chiasm

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6
Q

Causes of post-chiasmiatic lesions

A

Stroke
Anterior choroidal artery infarction
Multiple sclerosis (or other demyelinating disease)
Trauma
Internal capsule stroke (eg. basilar artery)
Haemorrhage
MCA stroke (lenticulostriate arteries)
PCA stroke
PRES (posterior reversible encephalopathy)

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7
Q

What are the expected findings of a prechiasmatic CN II (Optic) lesion?

A

Unilateral blindness and unilaterally unreactive pupil

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8
Q

What are the expected findings in a CN II (Optic) chiasma lesion

A

Bitemporal hemianopsia

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9
Q

What are the expected findings in a postchiasmatic CN II (optic) nerve lesion?

A

Homonymous hemianopia or quadrantanopia depending on the location of the lesions
+/- Macular sparing (Occipital cortex)

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10
Q

What are the expected findings in a CN III (Oculomotor) nerve lesion?

A

Ptosis (inferolateral displacement of the ipsilateral eye)
Dilated non-reactive pupil (to contralateral light reflex and accommodation) [note, Argyll Robinson Pupil accommodates but does not react]

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11
Q

What are the causes of CN III palsy (CN III = Oculomotor)

A

Diabetes (pupillary sparing)
Other causes of mononeuritis
Midbrain lesion, vascular, demyelinating
Basilar skull fracture
Uncal herniation as a result of increased intracranial pressure
SOL in the cavernous sinus
Syphilis (argyll Robinson)
Aneurysms (post communicating artery)

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12
Q

What are the expected findings in CN IV (Trochlear) palsy?

A

Weakness of downward eye movement with consequent vertical diplopia that is worse in the adducted eye position, but improved diplopia with head tilted to contralateral side

Weakness of intorsion, in particular with the eye abducted

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13
Q

What are the causes of CN IV (Trochlear) lesion?

A

Diabetes (mononeuritis)
Fracture of the sphenoid wing
Intracranial haemorrhage
Aneurysm (post communicating artery)
Midbrain lesion, vascular, demyelinating
Masses or tumours in the cavernous sinus

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14
Q

What are the expected findings in a CN V palsy?

A

Sensory abnormality

  • Peripheral nerve OR
  • Brain stem distribution

Motor abnormality:
- Asymmetry of jaw on opening or weakness with mastication

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15
Q

What are the causes of CN V (Trigeminal) lesion?

A

Trauma with skull fracture
Pontine lesions, vascular, demyelinating, tumour in pons and cerebellopontine angle eg. acoustic neuroma
Facial surgery - disturbance of peripheral branches of the sensory component
Cavernous Sinus lesions (upper 2 segments)

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16
Q

What are the expected findings of CN VI (Abducens) palsy

A

Medial deviation of ipsilateral eye

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17
Q

What are the causes of CN VI (Abducens) lesion

A

Wernicke’s (unilateral or bilateral)
Mononeuritis
Lesions in the cavernous sinus
Fractures of skull base
Raised intracranial pressure
Lesions in pons (vascular or demyelinating), cerebellopontine angle (eg. acoustic neuroma)
Idiopathic

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18
Q

What is the most common cause of CN palsy?

A

Diabetes

Other possibilities include:

  • Aneurysm
  • Vascular event
  • Mass lesion
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19
Q

Describe internuclear ophthalmoplegia?

A

Due to a lesion in the medial longitudinal fasiculus (heavily myelinated tract that runs between CN III and CN VI)

Findings:

  • Ipsilesional adduction deficit (partial or complete)
  • Contralateral, dissociated, horizontal abducting saccade/nystagmus on attempted gaze to the contralesional side.
  • Slow adducting saccadic velocity in the affected side.
  • Skew deviation with the ipsilateral hypertropic eye may be noted.
  • Vertical gaze nystagmus may be noted on upgaze.
  • The INO can be unilateral or bilateral and may present with or without (neurologically isolated) other brainstem findings.
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20
Q

Causes of horizontal gaze palsies

A
  • Frontal lobe lesions: deviation of eyes away from hemiparetic side and towards affected hemisphere
  • Pontine gaze centre lesions: deviation of eyes towards the hemiparetic side, contralateral to the pontine lesion
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21
Q

Causes of complex ophathlmoplegia

A

Myasthenia
Graves eye disease
Mitochondrial myopathies

22
Q

Which nerves are involved in cavernous sinus lesions

A

Sympathetic
CN III
CN IV
CN V (ophthalmic and sometimes maxillary divisions)
CN VI

Carotid artery
Ophthalmic veins

23
Q

Causes of cavernous sinus lesions?

A

Metastatic tumors
Localized spread of tumor: nasopharyngeal, pituitary
Primary intracranial tumors: meningiomas, neurofibromas
Carotid artery aneurysm
Carotid-cavernous fistula
Cavernous sinus thrombosis Eg. Bacterial, secondary to sinusitis, facial cellulitis
Miscellaneous inflammatory syndomres: Sarcoidosis, fungi/parasites (immunocompromised)

24
Q

Features of Myotonic Dystrophy?

A
  • *Muscle**
  • Myotonia (slow relaxation of hand grip, becomes less with muscle atrophy)
  • Weakness of: Distal > Proximal
  • Neck muscles (flexors and sternocleidomastoid)
  • Distal limb muscles, intrinsic muscles of hand, foot (foot drop)
  • Proximal usually stronger, but in some selective atrophy and weakness of quadriceps
  • Palatal, pharyngeal and tongue involvement, swallowing and speech problems, dysarthria and nasal speech
  • Diaphragmatic and intercostal muscle involvement may cause respiratory problems
  • Subgroup with proximal weakness
  • *Facial features:**
  • Frontal baldness
  • “Hatchet face” due to temporalis, masseter and facial muscle weakness and atrophy

Other:

Cardiac: Conduction problems, CHB; CCF; MVP

Intellectual impairment

Cataracts (multicoloured)

Drowsiness

Insulin resistence

Gonadal atrophy

Oesophageal and colonic reduced motility

25
Q

Parkinson’s disease - examination

A

Gait
Stooped, small steps, festinated, loss of arm swing, difficulty turning

Loss of balance (pull test)

Upper limbs

Hand tremor: resting, coarse, pill-rolling, asymmetrical. Improves with intention worsens when walking.

Bradykinesia: Progressive reduction in amplitude of movements, Eg. touch thumb to each finger (Decrementing movements), piano fingers, open/close fists

Primitive reflexes: Palmar-mental; grasp reflex

Head/Face

Mask-like face

Glabellar tap

Eye movements, saccades (PSP), gaze palsy

Other: voice, micrographia, postural BP, MMSE

26
Q

Parkinson plus - how to differentiate from PD?

A

PSP (Eye signs - saccades, gaze palsies)

MSA (Autonomic dysfunction, do a postural BP)

27
Q

What is the clinical significance of Pes Cavus?

A
  • Pes Cavus is due to atrophy of the intrinsic muscles of the feet
  • Appearance = high arch, claw toes, feet look thicker
  • Causes:
    • CMT (Hereditary motor and sensory neuropathy)
    • Friedreich’s
    • Other spinocerebellar degenerative disease
    • Childhood neuropathies, spina bifida
    • Idiopathic
28
Q

UMN findings with upper and lower limbs affected

Unilateral

Sensory findings present

What is the ddx?

A

Stroke/Central lesion/Cortical/subcortical

Brainstem

Spinal cord (Brown Sequard)

29
Q

UMN findings with upper and lower limbs affected

Bilateral

With sensory findings

A

Spinal cord compression (look for sensory level. Arms = cervical level)

MS (sensory findings variable, may have cerebellar findings)

B12 deficiency

Multiple CVAs

Arnold Chiari malformation (will also have cerebellar signs)

30
Q

UMN findings

Upper and lower limbs affected

Bilateral

No sensory findings

A

Cerebal palsy

MND (should see mixed UMN and LMN)

Multiple CVAs, often lacunar

31
Q

UMN findings

Lower limbs only (upper limbs normal)

A

Cerebral palsy (may selectively affect lower limb fibres)

Spinal stenosis below cervical spine

Parasagittal tumours, meningiomas

Hydrocephalus

Hereditary Spastic Paraparesis (sensory findings often mild)

32
Q

UMN signs

+ Ataxia

+/- sensory findings

A

Spinocerebellar degeneration

MS

Ataxic hemiparesis (lacune in upper pons/internal capsule)

Arnold Chiari Malformation

33
Q

LMN findings

No sensory loss

A

Polio Kennedy syndrome

34
Q

LMN findings

Sensory loss

A

Peripheral nerve

Nerve root compression

Cauda equina syndrome

Plexopathies

Peripheral neuropathies (sensorimotor)

35
Q

LMN peripheral neuropathy f

Areflexia

Distal weakness

Patchy sensory loss

A

Acute Guillian Barre

CIDP

Heredeitary neuropathy (CMT)

36
Q

LMN peripheral neuropathy

Areflexia

Sensory involvement

Little motor loss

A

Diabetes

Alcohol

Drugs eg. Vincristine

CKD

Paraneoplastic

Vit B12 deficiency

37
Q

Differentials for absent ankle jerk and upgoing plantar

A

MND (UMN and LMN findings)

Dual pathology - peripheral neuropathy and UMN lesion (sensory findings)

Friedreich’s Ataxis

Subacute combined degeneration (B12 deficiency)

38
Q

UMN signs

A

Spastic tone

Hyperreflexia

Positive Babinski

No atrophy

No fasciculations

39
Q

LMN signs

A

Flaccid tone

Atrophy present

Absent reflexes

Absent Babinski

Fasciculations present

40
Q

What are the causes of positive Romberg’s test?

A
  • Posterior column lesion
  • Peripheral neuropathy (especially affecting JPS)
  • Vestibular dysfunction (associated with ataxic gait)
41
Q

What are the expected LL neuro findings in diabetic peripheral neuropathy?

A

Bilateral distal sensation loss in a stocking distribution.

Absent ankle jerk

Romberg +ve (not always)

Sensory ataxic gait

42
Q

What are the expected LL neuro findings in CIDP?

A

Symmetrical sensorimotor neuropathy

Distal + proximal involvement

Romberg +ve (not always)

Reflexes absent

Muscle atrophy

43
Q

What are the expected LL neuro findings in multiple sclerosis?

A

Predominantly motor UMN findings:

Hyperreflexia (though reflexes may be lost due to interruption of motor reflex arc fibres)

Spasticity

Up-going plantar

+/- cerebellar findings

+/- sensory (patchy)

44
Q

What are some differential diagnoses for a bilateral symmetric spastic gait?

A

Bilateral stroke

Hereditary Spastic Paraplegia (HSP)

Spinal cord lesion

Cerebral palsy

Multiple sclerosis

45
Q

What are some differential diagnoses for bilateral foot drop

A

Peripheral sensorimotor neuropathy eg. CIDP, Charcot Marie Tooth

Bilateral strokes

Motor neuron disease

46
Q

What are some differential diagnoses for Parkinsonian-like gait

A

Parkinsonism: shuffling gait, stooped posture, loss of arm swing, tremor

Parkinson like syndromes: PSP, drug induced parkinsonism (posture upright)

47
Q

What are the differential diagnoses for wide-based gait?

A

Cerebellar ataxia

Sensory ataxia

Vestibular ataxia

Frontal ataxic gait (unlikely in exams)

48
Q

What are the likely causes for an asymmetric gait?

A

Unilateral spasticity eg. motor stroke

Unilateral cerebellar lesions

Unilateral foot drop (eg. Common peroneal nerve lesion, L5 lesions, unilateral stroke)

49
Q

Which conditions are pes cavus seen in?

A

Charcot Marie Tooth

Friedrich’s Ataxia

50
Q

Which nerve roots are responsible for knee and ankle reflexes?

A

Knee: L3, 4

Ankle: S1, 2

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