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Neurology - pathology > Neuro Qs > Flashcards

Neuro Qs Flashcards

1
Q

What is a seziure? What is epilepsy?

A

Seizure = convulsion or transient event caused by a paroxysmal discharge of cerebral neurones

Epilepsy = continued tendency to have seizures

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2
Q

How is epilepsy treated?

A

Primary generalised - valprate or lamotrigine

Absence seizure - valproate or ethosuxamide

partial seizure - carbamazepine, lamotrigine

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3
Q

How would you diagnose epilepsy? What specific sign would you see in a petit mal seizure?

A

Electroencephalography and CT/MRI (structural abnormalities?)

Genetical testing in Juvenile myoclonic epilepsy

3 Hz spike and wave for petit mal (absence seizures)

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4
Q

Give a side effect for each anti-epileptic drug you may prescribe

A

Sodium valproate – nausea, diarrhoea, weight gain

Lamotrigine – Steven-Johnson syndrome, diplopia, blurred vision

Carbamazepine – Steven-Johnson syndrome - SEVERE SKIN REACTION, hyponatraemia, impaired balance

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5
Q

What the triad of parkinson’s disease? Name 3 extra neuro symptoms

A

Triad = pill rolling tremor, bradykinesia, rigidity (postural instability and gait small shuffling)

Others= depression, anosmia, hallucinations, constipation, frequency

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6
Q

What causes Parkinson’s disease (pathophysiology)

A

Progressive degeneration of dopaminergic neurons in the sunstantia nigra pars compacta of the basal ganglia, associated with the presence of Lewy bodies.
This causes a decrease in striatal dopamine levels (and melanin) leading to cell loss and akinesia

(smoking is protective!!)

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7
Q

Describe the treatment of Parkinson’s disease, what side effects are associated?

A
  1. Levodopa + decarboxylase inhibitor e.g. carbidopa
    (Levodopa is a precursor of dopamine and can cross the BBB, the decarboxylase inhibitor prevents peripheral conversion of levodopa which reduces SE of N/V, arrhythmias, alopecia and hypotension. There is reduced efficacy over time so L-dopa should only be started when other treatments are ineffective.
  2. Dopamine agonists e.g. ropinirole
    SE: drowsy, nausea, hallucinations, compulsive behaviour
  3. Monoamine oxidase B inhibitors (MAOB-I) e.g. selegiline, rasagiline - reduces dopamine breakdown
    SE: postural hypotension, AF
  4. COMT inhibitors e.g. entacapone
    reduces breakdown of dopamine
    SE: can cause liver damage
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8
Q

What is Lewy body dementia?

A

When dementia occurs prior to or at the same time as motor symptoms
If dementia occurs more than 1 year after motor symptoms occur then it is a feature of Parkinson’s disease

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9
Q

What symptoms are seen in Huntington’s? What is diagnosis reached?

A

Mean onset is 30-50years

Symptoms: progressive, often begins with psychotic and behaviour symptoms, chorea (jerky movements, fidgidity movements, restlessness), lack of coordination, slow saccadic eye movements
Progressives to rigidity, dysphagia and behaviour change - aggressive, depression, self-neglet

Diagnosis: clinical, genetic, imaging - may show caudate nucleus atrophy and increase size of lateral ventricles

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10
Q

What is the pathophysiology of Huntington’s disease?

A

AD mutation in chromosome 4- huntingtin gene leading to huntintin protein overexpression (CAG repeats)

Cerebral atrophy of caudate nucleus and putamen of basal ganglia
- loss of corpus striatum GABA-nergic and cholinergic neurons - decreased ACh synthesis and GABA in the striatum
(dopamine levels are normal, high somatostatin, reduced ACh synthesis, depleted GABA and ACE in corpus striatum)

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11
Q

What is the treatment of Huntington’s disease?

A

SYMPTOMATIC
(Counselling/genetic testing)

  1. Benzodiazepams - diazepam
  2. Sodium valproate - anticonvulsant
  3. Tetrabenazine - used in hyperkinetic movement, promotes the degradation of dopamine, helps chorea
  4. Mood stabilisers e.g. carbamazepine
  5. Antidepressant e.g. amitriptyline

Also: speech therapy, physio, occupational therapy, pschyo therapy etc

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12
Q

What may trigger a tension headache? (3)
How may a patient describe the headache? (2)
Describe the management (2)

A

Triggers: stress, anxiety, noise, fumes, concentrated visual efforts
Headache is: bilateral, ‘tight band like sensation’
+- tenderness (no vomiting, aura)

Management: clinical diagnosis, life style: exercise, avoid triggers, NSAIDS, acupuncture
Consider amitriptyline

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13
Q

What may trigger a migraine? (3)
How may a patient describe the headache? (2)
Describe the management (2)

A

Triggers: cheese, caffeine, alcohol, menstruation, oral contraceptives, anxiety, travel, exercise (F>M, onset < 40yrs)

5+ Headaches: unilateral, lasts 4-72hrs, pulsatile/throbbing, aggravated by movement, nausea +- vomiting, photophobia/phonophobia

Management: avoid triggers, oral triptan (e.g. sumatriptan), NSAIDS, anti-emetic if needed e.g. metoclopramide
Prophylaxis - BB - e.g. propanolol
Consider amitriptyline

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14
Q

Clinical features of cluster headache? (2)
Name 2 features specific to the eye (2)
Name an acute and a chronic/prophylactic treatment

A

Clinical features: rapid onset, rises on crescendo over minutes and lasts 15-160 mins, very severe, occurs in clusters (1/2 x a day), +- vomiting

Eye symptoms: Lacrimation, miosis, transient ipsilateral Horner’s, lid swelling, unilateral eye pain, may awake pt from sleep +- ptosis

Tx

acute: 100% oxygen, sumatripitan (s/c) at onset
chronic: verapamil CCB, avoid alcohol, prednisolone

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15
Q

3 clinical features of giant cell arteritis (GCA) (3)

A

GCA: temporal pulsating headache, scalp tenderness, artery has reduced pulsating and is tender/pulseless, jaw claudication, amaurosis fungax - typically in one eye
Systemic: fatigue + fever, breathless, myalgia, morning stiffness

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16
Q

3 causes of spinal cord compression

What is the most common

A

Most common - disc herniation at L4/L5

Secondary malignancy – breast, lung, prostate, thyroid, kidney
TB – Pott’s disease = destruction of vertebral bodies and disc spaces
Epidural haemorrhage or haematoma
Prolapsed disc – usually L4/5 or L5/S1

MYELOPATHY = CORD COMPRESSION = UMN
RADICULOPATHY = ROOT COMPRESS = LMN
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17
Q

What occurs in Brown Sequard syndrome?

A

Hemisection of spinal cord results in..

Contralateral loss of pain and temperature
Ipsilateral loss of proprioception, vibration and power

18
Q

What occurs in Cauda Equina syndrome?

What investigation is gold standard? And what should you do?

A

Nerve root compression caudal to the termination of the spinal cord - usually large central disc herniation L4/L5, OR L5/S1
Generally S1-S5 = important in bladder function

WITHIN 24 HOURS
MRI – refer to neuro - surgery (epidural steroid injection)

19
Q

What symptoms are in cauda equina syndrome?

A 
Bilateral/unilateral pain in legs
Variable leg weakness
Saddle anaesthesia  (loss of sensation around buttock, perineum, inner thigh)
Poor anal tone
Erectile dysfunction
Bladder/bowel dysfunction
20
Q

Name 4 causes of TIA

A

Mostly due to micro emboli - Atrial fibrillation, atherosclerosis thrombi, vasculitis, antiphospholipid syndrome, thrombophilias, sickle cell, polycythaemia

21
Q

Describe the management of TIA

iv and rx

A

Brain imaging: MRI
Carotid doppler
ECG - AF?
ABCDD - age > 60, BP > 140/90, clinical weakness = 2, speech impairment = 1, duration 10-59mins = 1, >60mins = 2, DM?

TX: 2 weeks of aspirin than life long clopidogrel
Start satin, and don’t drive for 4 weeks.
Life style: stop smoking, diet, exercise, HTN control etc

22
Q

Describe the Oxford/Bamford classification of strokes, which vessels are affected?

A

Total anterior circulation stroke (TACS): middle cerebral artery, anterior cerebral artery

  1. Unilateral weakness (and/or sensory deficit) of face, arm, leg
  2. Homonymous hemianopia
  3. Higher cerebral function - dysphasia, visuospatial

Posterior anterior circulation stroke: middle cerebral artery and anterior cerebral artery, 2 of the three for TACS

Posterior circulation syndrome (POCS), one of: cerebellar or brainstem syndromes

  1. Loss of consciousness
  2. Isolated homonymous hemianopia

Lacunar syndrome (LACS): subcortical (midbrain, internal capsule) one of…

  1. Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg, or all three
  2. Pure sensory loss
  3. Ataxic hemiparesis (Cerebellar and motor syndrome)
23
Q

What are the 5 types of lacunar stroke?

A
  1. Motor
  2. Ataxia hemiparesis
  3. Sensory
  4. Mixed
  5. Dysarthria
24
Q

Describe the management of a cerebrovascular accident

A

URGENT CT - to direct treatment - an infarction is seen as a low density lesion

  1. WITHIN 4.5 hrs - THROMBOLYSIS - IV tissue plasminogen activator e.g. alteplase
  2. AFTER 24 hrs - ANTIPLATELET e.g. clopidogrel

(If after 4.5 hours then give aspirin for 2 days, then clopidogrel)

25
Q

Subarchnoid haemorrhage

  1. Clinical features
  2. Cause?
  3. Ix?
  4. Tx?
A
  1. Sudden onset thunderclap headache, neck stiffness, Kernig’s sign, altered level of consciousness, drowsiness, collapse, seizure, papilledema
  2. Most often berry aneurysm (HTN) - anterior communicating artery
  3. CT - star shaped
    LP - bloody then becomes yellow - XANTHOCHROMIC due to Hb break down to Hb
  4. Dexamethasone to decrease oedema, refer to neuro for clipping or coiling urgent. Nimodipine to reduce risk of vasospasm.
26
Q

What is Kernig’s sign?

A

Stiffness of hamstrings causes an inability to straighten the leg when hip is at 90 degrees

27
Q

Subdural haemorrhage

  1. Cause?
  2. Clinical features
  3. Who?
  4. Ix?
  5. Tx?
A
  1. Usually due to head injury, there is a latent stage when the tearing of bridging veins causes a haematoma to form, increasing ICP and shifting the midline structures - lucid period days/weeks/months
  2. raised ICP = headache, nausea, vomiting, raised BP, confusion, seizures, focal neurology (GCS), cognitive decline, personality change
  3. More common in elderly and alcoholics due to cerebral atrophy, physical abuse in infants
  4. CT - hyperdense crescent shape/sickle shape (becomes isodense then hypodense)
  5. Surgery - craniotomy - mannitol if raised ICP
28
Q

Extradural haemorrhage

  1. Cause?
  2. Clinical features
  3. Who?
  4. Ix?
  5. Tx?
A
  1. Head trauma - most commonly due to fracture of the temporal or parietal bone - laceration of middle meningeal artery (blood accumulates between bone and dura)
  2. Brief post-traumatic loss of consciousness
    Lucid period for several hours/days, followed by altered consciousness. Severe headache, nausea and vomiting, confusion, seizures, neuro deficit - may lead to rapid increase in ICP
  3. Often YP - trauma
  4. CT - hyperdense biconcave/egg shaped (XR may show fracture)
  5. Surgery - craniotomy - mannitol if raised ICP
29
Q

What is the cauda equina?

A

A bundle of spinal nerves and spinal nerve roots that consist of L2-5, S1-5 and coccygeal nerve, they innervate the lower limbs and pelvic organs. They also supply the sensory innervation to the perineum and parasympathetic supply to the bladder

30
Q

Describe the pathophysiology of MS

A

Inflammatory process in the white matter of the brain and cord mediated by CD4 T cells

In active lesions, there is an increase in inflammatory cells, active myelin degradation and phagocytosis; it heals incompletely causing relapsing and remitting
Plaques are not seen in peripheral nerves
Acute relapses are caused by focal inflammatory demyelination

31
Q

What clinical features are seen in MS? Which signs?

A

Brainstem – diplopia, vertigo, facial numbness/weakness, dysarthria or dysphagia
Spinal cord – spastic paraparesis, urinary symptoms

Lhermitte’s sign
By bending the head forward, the patient feels an electrical sensation down the back and limbs – due to lesion of dorsal columns

32
Q

What is McDonald Criteria?

A

MS - Uses frequency of attacks and lesions (MRI - disseminated in time and space) to diagnose MS

e.g. 1 attack + 1 lesion + MRI of lesions disseminate in time and space or 2 attacks + 2 lesions - more than one potential relapse

33
Q

What investigations for MS?

A
  1. Electrophysiology: delayed nerve conduction studies
  2. MRI - periventricular lesions - discrete white matter abnormalities
  3. LP - increased protein levels, oligoclonal IgG bands
34
Q

Treatment for MS

A

Relapse: oral methylprednisolone for 5 days OD or IV

DMARDS: Alemtuzumab - CD52 monoclonal antibody , dimethyl fumarate, natalizumab

Symptom management: Spasticity (Physio, baclofen, benzodiazepines), Botox injection and intermittent self catheterisation- for urgency and frequency, incontience - anticholinergic drugs e.g. doxizosin

35
Q

Courses of MS (4)

A

Relapsing and remitting

Secondary progressive – so starts as R+R

Primary progressive

Progressive relapsing

36
Q

Myasthenia gravis is an autoimmune condition, explain how the pathophysiology works

A

There is an autoimmune reaction producing antibodies to nicotinic acetylcholine receptors which interfere with neuromuscular transmission by depleting receptor sites. Immune complexes of anti-acetylcholine receptor IgG and complement are deposited at the post- synaptic membranes. There is a second group of antibodies against muscle specific receptors, tyrosine kinase (anti-MUSK)
Associated with thyroid disease, RA, pernicious anaemia and SLE

37
Q

What treatment causes a transient form of the condition?

A

Penicillamine (used in Wilson’s disease as a chelating agent)

38
Q

Describe the clinical features of Myasthenia gravis

A
  1. Weakness and fatiguability - ask pt to count to 50 - voice becomes less audible
  2. Begins in proximal muscles
  3. Also affects extra ocular muscles, facial expression and mastication, speech, fatiguable weakness - diplopia, ptosis
  4. Acute resp failure due to weakness of resp muscles
  • no muscle pain, sensory change, normal tone, no wasting, normal reflexes - but may be fatiguable - does not affect peripheral muscles
  • Ask to look up high to look at finger - eyes will drop after a few seconds
  • worsened by pregnancy/infection/BB
39
Q

Investigations for Myasthenia gravis

A

Ix

  1. Serum antibodies - anti-AChR or anti-MuSK (muscle-specific receptor tyrosine kinase)
  2. CT of thymus - hyperplasia in 70% - may due to a tumour
  3. Tensilon test - IV edrophonium given (short acting anti cholinesterase inhibitor) and power increases within seconds - rarely used for diagnosis
  4. Neurophysiology - reduced evoked muscle action potentials during repeated nerve stimulation
40
Q

Treatment of Myasthenia gravis

A
  1. Symptom control: oral acetyl cholinesterase inhibitors, e.g. pyridostigmine, neostigmine – duration of action 3-4 hours, prolong the action of ACh. Have cholinergic side effects: increased salivation, lacrimation, sweats, vomiting, diarrhoea, miosis
  2. Immunosuppression can be used to treat relapses or if there is no response to pyridostigmine – reducing regimen of prednisolone
  3. Azathioprine or methotrexate may also be given as the disease becomes more general
  4. Thymectomy if onset <50 years and disease not easily controlled, or if a thymoma is found on CT.
  5. Plasmapheresis or IVIg may be of use during severe exacerbation.
41
Q

What syndrome mimics myasthenia gravis and what is it caused by?

A

Lambert – Eaton syndrome, paraneoplastic manifestation of small cell bronchial carcinoma due to defective Ach release at neuromuscular junction. The difference is there are absent reflexes and autonomic involvement - dry mouth, constipation, impotence. Manage with immunoglobulins..

Neurology - pathology (11 decks)

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