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RACP Clinical Exam > Neurology > Flashcards

Neurology Flashcards

1
Q

Differentials for UMN findings with both upper and lower limbs affected
Unilateral, ± sensory findings

A
  • Stroke/other central lesions, cortical, subcortical, brainstem.
    • Spinal cord (Brown Séquard).
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2
Q

Differentials for UMN findings in lower limbs & LMN pathology findings in upper limbs

A

• Cervical syringomyelia-with sensory findings.
Cervical lesions with nerve roots affected in upper limbs and cervical spine stenosis causing UMN findings in lower limbs-with sensory findings
Syphilis

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3
Q

Differentials for UMN findings with both upper and lower limbs affected

Bilateral with sensory findings

A
  • Spinal cord compression (look for sensory level), if affecting arms and legs – cervical level, look for bladder/bowel problems.
    • MS (sensory findings variable, may have cerebellar findings).
    • B12 deficiency (UMN & Peripheral neuropathy).
    • Multiple CVAs.
    • Arnold Chiari malformation (cerebellar signs also).
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4
Q

Differentials for UMN findings with both upper and lower limbs affected

Bilateral with NO sensory findings

A

• Cerebral palsy.
• MND (should see a mix of UMN & LMN).
Multiple CVAs, often lacunar.

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5
Q

Differentials for UMN findings- lower limbs only (normal upper limbs)

A

• Cerebral palsy, may selectively affect lower limb fibers.
• Spinal stenosis below cervical spine (cervical spine stenosis may present with selective lower limb signs & sparing of the upper limbs).
• Parasagittal tumours, meningiomas.
• Hydrocephalus.
Hereditary Spastic Paraparesis (sensory findings often mild).

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6
Q

Differentials for UMN signs & ataxia (± sensory findings

A

• Spinocerebellar degeneration.
• MS.
• Ataxic hemiparesis (lacune in upper pons/internal capsule).
Arnold Chiari Malformation.

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7
Q

Differentials for findings of lower motor neurone pathology

A

LMN lesions: may be anywhere from anterior horn cells & distally i.e. nerve root, plexus or peripheral nerves.

LMN findings – no sensory loss:

Polio (often with underdeveloped limb, if occurring in childhood).

LMN findings and sensory loss:

Peripheral nerve.
Nerve root compression.
Cauda Equina Syndrome.
Plexopathies.
Peripheral neuropathies (sensorimotor).
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8
Q

Differentials for peripheral neuropathy

Findings of areflexia with distal weakness & some sensory loss

A

Acute Guillian Barre.
CIDP.
Hereditary neuropathy (e.g. Charcot Marie Tooth, CMT).

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9
Q

Differentials for peripheral neuropathy

Findings of areflexia with sensory involvement and little motor loss:

A 
Diabetes.
Alcohol.
Drugs e.g. vincristine.
Chronic kidney disease.
Paraneoplastic.
Vitamin B12 deficiency (may have UMN findings also e.g. up-going plantar).
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10
Q

Differentials for absent ankle jerk and upgoing plantar

A

MND (UMN & LMN findings).
Dual pathology, peripheral neuropathy & UMN lesion (sensory findings).
Friedreich’s Ataxia.
Subacute combined degeneration (B12 deficiency).

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11
Q

What are the expected lower limb findings in a patient with diabetic peripheral neuropathy?

A

Findings in diabetic neuropathy are dependent on the extent and severity of the sensory loss and may include:
Gait may be that of a sensory ataxia.
Romberg’s test may be +ve.
There is progressive loss of distal sensation in a glove and stocking distribution and in severe cases, motor weakness may be present.
Ankle jerks may be lost.

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12
Q

What are the expected lower limb findings in a patient with CIDP?

A

In its classic form, CIDP causes a symmetric, sensori-motor neuropathy with a predominant motor neuropathy that results in both proximal and distal muscle weakness.
Less common variants include asymmetric and/or sensory-predominant forms.
Reflexes are generally absent or reduced.
Typical findings include an ataxic gait with a +ve Romberg, loss of sensation in a glove & stocking distribution, muscle atrophy and weakness and globally absent/reduced reflexes.

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13
Q

What lower limb findings may be elicited in a patient with multiple sclerosis?

A

Lower limb findings include: UMN signs, hyper-reflexia, spasticity, up-going plantar. Occasionally reflexes are lost due to interruption to afferent motor reflex arc fibres. Cerebellar and sensory finding (which may be patchy) may also be present.

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14
Q

What are the causes for a +ve Romberg test?

A

A +ve Romberg test is where the patient is steady with their eyes open and unsteady with their eyes closed.
A +ve Romberg is in keeping with:
Posterior column lesion:
Peripheral neuropathy (in particular with loss of joint position sense).
Vestibular dysfunction (may be only finding, in addition to an ataxic gait) eg. aminoglycoside side effects

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15
Q

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

A 
Differentials for spasticity, i.e. bilateral UMN lesion include:
Bilateral stroke.
Hereditary Spastic Paraplegia (HSP).
Spinal cord lesion. 
Cerebral palsy.
Multiple Sclerosis (MS).
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16
Q

What are some differential diagnoses for bilateral foot drop?

A

Some differential diagnoses for bilateral foot drop include:
Peripheral sensorimotor neuropathy e.g. CIDP, Charcot Marie Tooth (CMT).
Bilateral strokes.
Motor neuron disease (MND).

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17
Q

What are some differential diagnoses for Parkinsonian - like gait?

A

Differentials include:
Parkinsonism: shuffling gait, stooped posture (upper limbs loss of swing & tremor).
Parkinson-like syndromes: e.g. Progressive Supranuclear Palsy, drug induced parkinsonism, posture is often more upright.

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18
Q

What are the differential diagnoses for wide-based gait?

A

Differential diagnoses for wide-based gait include:
Cerebellar ataxia.
Sensory ataxia.
Vestibular ataxia.
Frontal ataxic gait (unlikely in the exams).

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19
Q

What are the likely cause of an asymmetric gait?

A

Unilateral spasticity eg. motor stroke (circumduction, extension of the hip, knee and ankle, leg swings out in a lateral arc), upper arm adducted and internally rotated, elbow & wrist flexed

Unilateral cerebellar lesions (veering to a side)

Unilateral foot drop: common peroneal nerve lesion, L5 lesion, unilateral stroke

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20
Q

Differential diagnosis of muscle atrophy in lower limb neuro exam

A

Lower motor neuron lesions.
Peripheral nerve, plexus or root lesions.
Myopathies.

21
Q

Pes cavus (high arch and claw toes) may be seen in:

A

Charcot Marie Tooth.

Friedreich’s ataxia.

22
Q

What are the lower limb findings in an upper motor neuron lesion (UMN)?

A

Findings in UMN include:
Absence of muscle atrophy.
Absence of fasciculations.
Increased tone, spasticity or clasp knife tone with/without clonus.
Pattern of weakness: weaker anti-gravity muscles i.e. hip flexion weaker than hip extension, knee extension weaker than knee flexion, ankle dorsiflexion weaker than ankle plantarflexion.
Hyperreflexia.
Plantar reflex up-going.

23
Q

What are the lower limb findings in lower motor neuron lesions (LMN)?

A 
Findings in LMN lesions:
Muscle atrophy.
Fasciculations.
Decreased tone, flaccidity.
Pattern of weakness: hip extension weaker than hip flexion, knee flexion weaker than knee extension, ankle plantarflexion weaker than ankle dorsiflexion.
Hyporeflexia or areflexia.
Plantar reflex down-going.
24
Q

What are the lower limb findings in proximal myopathy?

A 
Findings in proximal myopathy:
Muscle atrophy in affected muscles.
No fasciculations.
Normal tone.
Pattern of weakness: Proximal muscles.
Normal reflexes.
Plantar reflex down-going.
25
Q

What are the lower limb findings in sensorimotor peripheral neuropathy?

A

In sensorimotor peripheral neuropathy there may be a variable mix of glove/stocking distribution sensory loss and motor weakness in a symmetric distribution.
Absent ankle jerks.

26
Q

What are the lower limb findings in cerebellar lesions?

A

Cerebellar ataxic gait.
Abnormal heel to shin test.
Dysdiadochokinesis (abnormal foot tapping).

27
Q

What are the findings in upper limb, upper motor neuron (UMN) lesion?

A

Findings in UMN lesions:
Absence of muscle atrophy.
Absence of fasciculations.
Increased tone, spasticity or clasp knife.
Pattern of weakness: Weaker anti-gravity muscles i.e. shoulder abduction weaker than shoulder adduction, elbow extension weaker than elbow flexion, wrist extension weaker than wrist flexion, finger extension weaker than finger flexion.
Hyperreflexia, including brisk finger jerk and a +ve Hoffman sign.

28
Q

What are the findings in upper limb, lower motor neuron (LMN) lesion?

A 
Muscle atrophy.
Fasciculations.
Decreased tone, flaccidity.
Pattern of weakness: Weaker pro-gravity muscles i.e. shoulder adduction weaker than shoulder abduction, elbow flexion weaker than elbow extension, wrist flexion weaker than wrist extension, finger flexion weaker than finger extension.
Hyporeflexia or areflexia.
29
Q

What are the upper limb findings in patients with cerebellar disease?

A

Findings in cerebellar lesions include:
Dysmetria, finger nose test.
Dysrhythmokinesis.
Dysdiadokinesis.

30
Q

Findings in 3rd CN palsy

A

Findings in palsy:
• Ptosis, inferolateral displacement of the ipsilateral eye.
• Reduced adduction, elevation and depression of the affected eye.
• A dilated non-reactive pupil (to direct or contralateral light reflex & accommodation). In diabetic mononeuritis pupillary sparing is often seen.

31
Q

Findings in 4th CN palsy:

A

Findings in palsy:
• 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 (look to the nose then down).
Weakness of intorsion, in particular with eye abducted.

32
Q

Common cause of 3rd and 4th CN palsy:

A

• Tumours can compress the nerve anywhere along its path.
• Cavernous sinus lesions.
• Trauma.
• Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the midbrain.
• Mononeuritis multiplex e.g. diabetes (often with pupillary sparing).
Intracranial aneurysms, in particular posterior communicating artery aneurysms.

33
Q

Findings in CN 6th palsy

A

Findings in palsy:
• Medial deviation of ipsilateral eye.
• Inability to look laterally (abduct).

34
Q

Common causes of CN 6th palsy:

A

• Tumours can compress the sixth nerve anywhere along its path. Acoustic neuromas can affect the 6th nerve.
• Elevated intracranial pressure, a false localising sign.
• Trauma.
• Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons.
Mononeuritis multiplex e.g. diabetes.

35
Q

Findings in 5th CN palsy

A

Findings in palsy:
• Sensory abnormality with peripheral nerve OR descending nucleus distribution (pain & temperature).
• Motor abnormality: asymmetry of jaw on opening or weakness with mastication.
Loss of corneal reflex.

36
Q

Common causes of 5th CN palsy:

A
  • Tumours can compress the nerve anywhere along its path.
    • Trauma.
    • Cavernous sinus lesions can affect the two superior divisions of the trigeminal nerve.
    • Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons or along its descending nucleus.
37
Q

Findings in 7th CN palsy:

A

Lower motor neuron lesions:
Weakness of upper and lower facial muscles.
Upper motor neuron lesions:
Weakness of lower facial muscles with sparing of upper facial muscles.
Loss of corneal reflex.
Decreased tearing
Hyperacusis.
Loss of taste sensation on the anterior 2/3rds of the tongue.

38
Q

Common causes of lower motor neuron CN 7th palsy:

A

Bell’s palsy, idiopathic facial nerve palsy or facial nerve palsy of suspected viral aetiology is the most common cause of peripheral, lower motor neuron facial nerve palsy.
Sarcoidosis.
Herpes zoster infection.
Guillain-Barré syndrome.
Otitis media.
Lesions affecting nucleus of facial nerve in ipsilateral pons, e.g. stroke, acoustic neuroma, demyelinating lesions.

39
Q

Common causes of upper motor neuron CN 7th palsy:

A

Lesion affecting the contralateral upper motor neuron fibres (above nucleus to cerebral motor cortex)

40
Q

Findings in CN 8th palsy

A

Hearing loss.

Vestibular ataxia.

41
Q

Common cause of 8th CN palsy

A

Acoustic neuroma.

Trauma or inflammatory conditions along it path.

42
Q

9th CN palsy findings

A

Loss of taste in the posterior 1/3rd of the tongue.

Loss of pain and touch sensations in soft palate, and pharyngeal walls.

43
Q

Findings in CN 10th Palsy

A

Uvula deviation towards normal palate, may result from ipsilateral lower motor lesion of the vagus nerve OR contralateral upper motor neuron vagus nerve.
Through the recurrent laryngeal nerve to the vocal cords, hoarseness may develop.
Dysphagia, dysphonia and decreased gag reflex.
Due to its parasympathetic input, cardiac and gastrointestinal abnormalities may be seen with vagal lesions

44
Q

Common cause of CN 10th palsy

A

Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla.
Upper motor lesions of the 10th nerve tract, often as a component of a pseudobulbar palsy.
Motor neuron disease.

45
Q

Findings in CN 11th palsy

A

Paralysis of sternocleidomastoid and trapezius.

46
Q

Common cause of 11th CN palsy

A

Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla

47
Q

Findings in 12th CN palsy

A

Protrusion of tongue away from side of lesion for an upper motor neuron process and toward the side of the lesion for a lower motor neuron process.

48
Q

Common cause of palsy

A

Trauma.
Tumour along its path.
Stroke (e.g. medial medullary syndrome), demyelinating lesions and tumours affecting the nucleus in the medulla.
Upper motor lesions of the 12th nerve tract, often as a component of a pseudobulbar palsy.
Motor neuron disease.

49
Q

Differentials in complex ophthalmoplegia include

A

Myasthenia gravis.
Mitochondrial myopathies.
Graves eye disease.

RACP Clinical Exam (4 decks)

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