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Neurology Flashcards

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1
Q

Explain the cause of myotonic dystrophy

A

Genetic condition with two types depending on gene defect.
Autosomal dominant and shows genetic anticipation

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2
Q

Name three neurological conditions that exhibit genetic anticipation

A

Myotonic dystrophy
Huntington’s chorea
Friedrich’s ataxia

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3
Q

Name causes of bilateral ptosis

A

Congenital
Myasthenia gravis
Myotonic dystrophy

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4
Q

Name causes of unilateral ptosis

A

Third nerve palsy
Horner’s syndrome

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5
Q

Name non-neurological issues associated with myotonic dystrophy

A

Cataracts
Cardiomyopathy
Arrhythmia
Diabetes
Testicular atrophy
Dysphagia

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6
Q

How is myotonic dystrophy diagnosed?

A

Genetic testing - DMPK/ZNF9 gene
EMG - dive bomber potentials

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7
Q

Name some causes of unilateral cerebellar syndrome

A

Demyelination, ie multiple sclerosis
Stroke - posterior infarct or haemorrhagic
Tumour
Multiple system atrophy

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8
Q

Name some causes of bilateral cerebellar syndrome

A

Demyelination, ie multiple sclerosis
Paraneoplastic syndromes
Bilateral posterior circulation stroke
Tumour
Multiple system atrophy
Drugs eg phenytoin, lithium, carbamazepine
Alcohol
Metabolic conditions eg wilsons, b12 deficiency, hypothyroidism
Infections eg lyme disease, HIV, syphilis
Miller fisher GBS (inflammatory)
Hereditary eg friedrich’s ataxia, ataxic telangiectasia
Neurofibromatosis

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9
Q

Name signs found in cerebellar syndrome

A

Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Slurred or staccato speech
Hypotonia/hyporeflexia

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10
Q

What is most likely underlying condition if patient has cerebellar signs AND internuclear ophthalmoplegia and spasticity

A

MS

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11
Q

What is most likely underlying condition if patient has cerebellar signs AND clubbing, tar stained fingers

A

Bronchial carcinoma

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12
Q

What is most likely underlying condition if patient has cerebellar signs AND stigmata of liver disease?

A

Alcoholic cerebellar degeneration

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13
Q

What is most likely underlying condition if patient has cerebellar signs AND neuropathy?

A

Alcoholic cerebellar degeneration
Friedrich’s ataxia

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14
Q

What is most likely underlying condition if patient has cerebellar signs AND gingival hyperplasia?

A

phenytoin toxicity

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15
Q

How is multiple sclerosis diagnosed?

A

CNS demyelination disseminated in space and time
MRI - white matter plaques
CSF - oligoclonal IgG bands. Increased protein
Visual evoked potentials - delayed velocity but normal amplitude

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16
Q

What is the sign of internuclear ophthalmoplegia?

A

eg if lesion on left, on looking to the right right eye has nystagmus and left eye is unable to adduct. both eyes look to left and converge normally.

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17
Q

How is multiple sclerosis managed?

A

MDT approach
Nurses, physio, OT, social worker, physician
Chronically - interferon beta reduce relapse rate but not progression. Monoclonal antibodies can reduce disease progression. Antispasmodics, carbamazepine for neuropathic pain
Acutely - methylpred to shorten duration

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18
Q

What are the clinical diagnostic criteria for a total anterior circulation stroke?

A

Unilateral weakness (and/or sensory deficit) of face AND arm AND leg
AND
Homonymous hemianopia
AND
Higher cerebral dysfunction

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18
Q

What are the clinical diagnostic criteria for a total anterior circulation stroke?

A

Unilateral weakness (and/or sensory deficit) of the face AND arm AND leg
AND
Homonymous hemianopia
AND
Higher cortical dysfunction

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18
Q

What are the clinical diagnostic criteria for a total anterior circulation stroke?

A
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19
Q

What blood vessel is involved in a total anterior circulation stroke?

A

middle and anterior cerebral arteries

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20
Q

What are the clinical diagnostic criteria for a partial anterior circulation stroke?

A

TWO of
Unilateral weakness (and/or sensory deficit) of face AND hand AND leg
Homonymous hemianopia
Higher cortical dysfunction

OR
Higher cortical dysfunction alone

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21
Q

What are the clinical diagnostic criteria for a posterior circulation stroke?

A

ONE of:

Cranial nerve palsy AND contralateral motor and/or sensory deficit
Homonymous hemianopia
Cerebellar dysfunction
Conjugate eye movement disorder
Bilateral motor or sensory deficit

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22
Q

What are the clinical diagnostic criteria for a lacunar stroke?

A

ONE of:
Sensory deficit
Motor deficit
Sensori-motor deficit
Ataxic hemiparesis
NO higher cortical dysfunction

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23
What are some acute and subacute complications of stroke?
Acute: Haemorrhagic transformation aspiration pneumonia Subacute: Pressure sores DVT PE Pneumonia
24
What is the immediate management of suspected stroke?
CT scan Depending on results and time since onset: If ischaemic and If large vessel occlusion and within 6 hours - discuss with IR re ?thrombectomy If within 4.5 hours - IV thrombolysis Admission to hyperacute stroke unit for MDT management Aspirin and PPI asap if no thrombolysis. Aspirin after 24 hours if thrombolysis for 2 weeks. If AF start anticoag after 2 weeks, otherwise switch aspirin to clopidogrel High dose statin after 48 hours IPCS for thromboprophylaxis
25
What is the long term management of stroke?
MDT approach After 2 weeks, switch aspirin to either clopi or anticoagulation High dose statin Blood pressure management if appropriate Physio SALT input
26
What are the signs involved in lateral medullary syndrome?
Loss of pain and temperature sensation CONTRALATERAL to the lesion Cerebellar signs/nystagmus/horner syndrome IPSILATERAL to the lesion
27
How does lateral medullary syndrome come about?
Occlusion of posterior inferior cerebellar artery or vertebral artery. Spinothalamic tract decussates below the point of the medulla, hence contralateral symptoms
28
What are the most common causes of a spastic paraparesis?
Demyelination, ie MS Cord compression Trauma Anterior horn cell disease, ie MND Cerebral palsy
29
What would be the common causes of a spastic paraparesis AND a sensory level?
Cord compression, due to trauma, tumour, abscess, haematoma Cord infarction Transverse myelitis, due to neuromyelitis optica, infection, autoimmune disease or sarcoid
30
What would be the suspected causes of spastic paraparesis AND loss of vibration sense and proprioception?
MS Friedrich's ataxia Syphilis Subacute combined degeneration of the cord Cervical myelopathy
31
What would be the suspected causes of spastic paraparesis AND loss of pain and temperature sensation?
Syringomyelia Anterior spinal artery infarction
32
What nerve roots control the patellar reflex?
L3/L4
33
What nerve roots control the ankle jerk reflex?
S1/S2
34
What nerve roots control hip flexion?
L2/L3
35
What nerve roots control foot dorsiflexion?
L4/L5
36
What is the aetiology of Charcot-Marie-Tooth disease?
Group of hereditary neuropathies. Different genetics depending on subtype, most often autosomal dominant or x-linked. CMT 1, 3 and 4 are demyelinating, whereas CMT 2 is an axonal pathology.
37
What are the presenting features and clinical signs of Charcot-Marie-Tooth disease?
Muscle wasting of small muscles of feet, progresses proximally, in time also affects the upper limbs. Distal to proximal sensory loss of all modalities, loss of proprioception can lead to sensory ataxia. Areflexia. CMT3 usually presents in infancy whereas CMT1 presents by 10 years and CMT2 in the second decade.
38
What are the differentials for a patient presenting with peripheral neuropathy?
Alcohol excess Diabetes mellitus B12 deficiency Thyroid disease Infection - HIV, syphilis Vasculitis Amyloidosis Heavy metal poisoning Drugs eg vincristine
39
What are the key investigations for peripheral neuropathy?
For underlying condition: check vitamins, thyroid, blood glucose/HbA1c, TFT, LFT, BBV screen, VDRL, serum protein electrophoresis. Nerve conduction studies In select cases, may also need: Nerve biopsy Imaging of central nervous system CSF analysis
40
What are the typical features of Guillain-Barre syndrome?
Progressive weakness of all 4 limbs Areflexia Near symmetrical Mild sensory symptoms, if any Autonomic dysfunction Often few weeks after infective illness High CSF protein
41
What are the clinical findings in syringomyelia?
At affected levels: -Weakness and wasting of small muscles of the hand -Loss of upper limb reflexes -Loss of pain and temperature sensation, preserved proprioception and vibration sense until later stages. Shawl like distribution. Below affected levels - upper motor neurone signs.
42
DDX for generalised wasting of hand muscles
Anterior horn cell - MND, syringomyelia, cervical cord comp, polio Brachial plexus injury Peripheral nerve - combined median and ulnar entrapment, peripheral neuropathy Disuse atrophy eg MSK conditions
43
What is chorea?
Movement disorder causing sudden uncontrollable movements of limbs and facial muscles.
44
Causes of chorea
Hereditary - Huntingtons, Neuroacanthocytosis, Wilson's, Benign hereditary chorea Immune - Sydenham's chorea, SLE Drug induced - phenytoin, carbamazepine, valproate, gabapentin, amphetamines, cocaine, methylphenidate, lithium, levodopa, dopamine agonists. Infection - AIDA, lyme disease Vascular - post infarct. Hormonal - hyperthyroidism, hypoparathyroidism, pregnancy
45
Investigations for chorea
Bloods - FBC, U and E, bone profile, Mg, LFT, TFT BBV screen, VDRL Immune - ESR, ANA Antistreptolysin O titre (if suspected trigger is strep infection) Caeruloplasmin and 24 hr urine copper MRI EEG - if need to differentiate seizures from involuntary movement
46
Features of Huntington's
Chorea Low tone Personality/mood change Occulomotor changes, slow saccades Dysarthria Ataxia Progressive
47
Genetics of Huntington's
Autosomal dominant 100% penetrance Usual onset around 40 years Diagnosed by number of CAG repeats, with >40 being unequivocally abnormal.
48
What is the pathophysiology of MS?
Acquired immune mediated inflammatory condition causing demyelination throughout CNS.
49
What are the patterns of MS?
Relapsing-remitting Secondary progressive Primary progressive
50
Investigations for MS
MRI LP - oligoclonal bands Visual evoked potentials
51
Presentation for MS
Can present with pretty much any neurology, commonly: -Monocular visual loss, painful eye movements (optic neuritis) -Diplopia -Sensory disturbance -Weakness -Balance issues -Transverse myelitis -Autonomic dysfunction
52
Management of MS
-Flares- methylprednisolone 5/7 -Disease modifying - interferon beta, glatiramer, MAbs -MDT - PT/OT -Lifestyle - smoking cessation, inform DVLA
53
What is the genetic basis of Friedrich's ataxia?
Autosomal recessive Mutation of Frataxin gene on chromosome 9; usually a repeat expansion Decreased frataxin protein results in oxidative damage to cells, primarily CNS and heart
54
Presentation in Friedrich's ataxia
Unsteadiness/incoordination is usually the presenting symptom Cardiomyopathy Scoliosis, pex cavus
55
What is the type of ataxia in Friedrich's ataxia?
Usually afferent, due to degeneration of dorsal root ganglia. May have dysarthria if CNs involved
56
Other neurology in Friedrich's ataxia
Extensor plantars Areflexia Pyramidal lower limb weakness Hearing loss, visual disturbances
57
Upper limb myotomes
C5 - elbow flexors C6- wrist extensors C7 - elbow extensors C8 - finger flexors T1 - finger abductors
58
Polio transmission route
Feco-oral
59
Polio incubation
2-35 days
60
What structure is affected by polio?
Predominantly anterior horn. Also posterior horn, thalamus, hypothalamus, brain stem.
61
What is post polio syndrome?
new, insidious onset of weakness, fatigue and pain with additional muscle atrophy years after the acute infection
62
What proportion of those with polio paralysis develop post-polio syndrome?
Over 2/3
63
What are the symptoms of post-polio syndrome?
Fatigue, myalgia, exercise intolerance, decreased endurance, joint pain Also cold intolerance and dysphagia
64
Cerebellar syndrome signs
Arms - dysdiadochokinesia, intention tremor, past pointing (dysmetria) Legs- ataxic gait, heel shin incoordination Face - nystagmus (towards lesion), slurring or staccato speech, titubation
65
Causes of sensory ataxia
Peripheral neuropathy, tabes dorsalis (DCML), Subacute degeneration of the cord, demyelination

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