Neurology Flashcards

1
Q

Describe symptoms of an extradural bleed

A
  • developed a headache after head trauma
  • confused and drowsy
  • difficult to rouse
  • biconvex shape on CT
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2
Q

What is an extradural haemorrhage?

A
  • usually caused by rupture of middle meningeal artery
  • in temporo-parietal region
  • associated with fracture of temporal bone
  • occurs between skull and dura mater
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3
Q

Where does a subdural haemorrhage occur?

A
  • rupture of bridging veins in outermost meningeal layer
  • occurs between dura mater and arachnoid mater
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4
Q

Describe the presentation of subdural bleeding

A
  • crescent shape on CT and possible midline shift
  • drowsiness, reduced consciousness, high ICP
  • seizure
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5
Q

What is the pathophysiology behind subdural bleeding?

A
  • usually occurs due to trauma
  • turning/jerking injuries cause damage to the bridging veins and causes tears
  • elderly and alcoholics have more brain atrophy making rupture more likely
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6
Q

Describe presentation of subarachnoid bleeding

A
  • sudden onset
  • severe thunderclap headache
  • occurs due to strenuous activity
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7
Q

What is Guillan-Barré syndrome?

A
  • an acute paralytic polyneropathy
  • affects peripheral nervous system
  • symptoms peak after 2-4 weeks, recovery can take months-years
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8
Q

What causes Guillan-Barré syndrome?

A
  • triggered by infection
  • associated with:
  • campylobacter jejuni (MC)
  • cytomegalovirus
  • Epstein-Barr virus
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9
Q

What is the pathophysiology behind Guillan-Barré syndrome?

A
  • occurs due to molecular mimicry
  • B cells create antibodies against antigens on the pathogen
  • these antibodies match proteins on nerve cells
  • Abs then target myelin sheath of motor nerve cell or nerve axon
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10
Q

How does Guillan-Barré syndrome present?

A
  • symmetrical ascending weakness (starting at feet)
  • reduced reflexes
  • peripheral loss of sensation/neuropathic pain
  • progresses to cranial nerves and causes facial weakness
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11
Q

How is Guillan-Barré syndrome diagnosed?

A
  • Brighton criteria
  • nerve conduction studies
  • lumbar puncture for CSF: raised protein, normal cell count and glucose
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12
Q

How is Guillan-Barré syndrome managed?

A
  • IV immunoglobulins
  • plasma exchange
  • supportive care
  • VTE prophylaxis
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13
Q

What is multiple sclerosis?

A
  • chronic and progressive condition involving demyelination of neurones in the CNS
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14
Q

What is the epidemiology of multiple sclerosis?

A
  • young adults (under 50)
  • more common in women
  • symptoms improve in pregnancy and postpartum
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15
Q

What is the pathophysiology of multiple sclerosis?

A
  • myelin provided by Schwann cells in PNS and oligodendrocytes in CNS
  • inflammation around myelin and infiltration of immune cells damages myelin causing symptoms
  • re-myelination can occur in early disease, is incomplete in late disease > permanence
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16
Q

Why do symptoms of MS change over time?

A
  • lesions vary in location over time
  • different nerves are affected and symptoms change
  • lesions are disseminated in time and space
  • early course: relapsing-remitting attacks
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17
Q

What is the aetiology of multiple sclerosis?

A
  • genetic
  • EBV
  • low vit D
  • smoking
  • obesity
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18
Q

What optical symptoms occur with multiple sclerosis?

A
  • double vision: abducens (VI) lesions
  • internuclear opthalmoplegia: problems with coordinating eye movements (III, IV, VI)
  • conjugate lateral gaze disorder: affected eye cannot abduct (VI)
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19
Q

What is optic neuritis?

A
  • unilateral reduced vision over hours to days
  • central scotoma (enlarged blind spot)
  • impaired colour vision
  • pain on eye movement
  • relative afferent pupillary defect
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20
Q

What is the general presentation of multiple sclerosis?

A
  • sensory and cerebellar ataxia
  • tremors
  • incontinence
  • limb paralysis
  • trigeminal neuralgia, numbness and paresthesia
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21
Q

How is multiple sclerosis diagnosed?

A
  • progressive symptoms over a year
  • or 2 attacks disseminated in time and space
  • MRI brain + cord showing lesions
  • LP shows oligoclonal IgG bands in CSF
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22
Q

What are the types of disease course of multiple sclerosis?

A
  • relapsing-remitting: episodes of disease followed by recovery - can be active and/or worsening
  • 1º progressive: gradual deterioration without recovery
  • 2º progressive: relapsing-remitting > worsening and incomplete remission
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23
Q

How is multiple sclerosis managed?

A
  • acute episodes: IV methylprednisolone
  • DMDs: β interferon
  • mitoxantrone
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24
Q

What are differential diagnoses for multiple sclerosis?

A
  • SLE, Sjrogen’s, encephalomyelitis
  • Lyme’s, syphilis, AIDS
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25
What is Parkinson's disease?
- progressive reduction of dopamine in the basal ganglia leading to movement disorders - substantia nigra produces dopamine - asymmetrical symptom
26
What are the risk factors and epidemiology of Parkinson's?
- family history - male - inc age - e.g. 70y/o male
27
What are the symptoms of Parkinson's?
- unilateral tremor: 4-6Hz - cogwheel rigidity: jerky movement - bradykinesia: shuffling gait, difficulty initiating movement, reduced facial expression - anosmia - postural instability
28
How is Parkinson's diagnosed and what is the classic triad?
- clinically based on symptoms - resting tremor, rigidity, bradykinesia - DaTscan
29
How is Parkinson's managed?
- Levodopa + decarboxylase inhibitor - dopamine agonist e.g. bromocriptine - COMT inhibitors e.g. entacapone: metabolises L-dopa - Monoamine oxidase B inhibitors - rasagiline
30
How does levodopa work and what are the associated side effects?
- synthetic dopamine e.g. carbidopa - taken alongside decarboxylase inhibitor e.g. benserazide - becomes less effective over time - leads to dyskinesias e.g. dystonia, chorea, athetosis
31
What is Huntington's chorea and what is the pathophysiology?
- autosomal dominant condition with full penetrance - trinucleotide repeat disorder in HTT in chromosome 4 - lack of GABA and excessive nigrostriatal pathway
32
What is genetic anticipation?
- more trinucleotide repeats leads to earlier onset of disease and increased severity
33
When does Huntington's present and what is the prognosis?
- asymptomatic until age 30-50 - life expectancy: 15-20yrs after onset of symptoms
34
How does Huntington's present?
- cognitive, psychiatric and mood problems > movement disorder - chorea - eye movement disorders - dysarthria and dysphagia - depression
35
How is Huntington's diagnosed?
- genetic testing with pre and post-test counselling - diagnosis if > 35 CAG repeats
36
How is Huntington's managed?
- antipsychotics e.g. olanzapine - benzodiazepines e.g. diazepam - dopamine-depleting agents e.g. tetrabenzine - antidepressants
37
What is myasthenia gravis?
- autoimmune condition causing muscle weakness - progressively worse weakness with activity which improves with rest - mostly affects proximal muscles and small muscles of head and neck
38
What is the epidemiology of myasthenia gravis?
- women under 40 - men over 60 (more related to thymoma)
39
What is the pathophysiology behind myasthenia gravis?
- Ach-R antibodies bind to postsynaptic NMJ receptors - Ach unable to bind, stimulate receptor and trigger muscle contraction - more used during activity and so more are blocked - Abs activate complement system leading to damage at postsynaptic membrane
40
How does myasthenia gravis present?
- extraocular muscle weakness > diplopia - eyelid weakness > ptosis - dysphagia - jaw fatigue - slurred speech - facial weakness
41
How can myasthenia gravis be examined?
- repeated blinking > ptosis - prolonged upward gazing > diplopia - repeated abduction of one arm > unilateral weakness
42
How is myasthenia gravis diagnosed?
- testing for antibodies: acetylcholine receptor (Ach-R) and muscle-specific kinase (MuSK) - Edrophonium test
43
What is the edrophonium test for myasthenia gravis?
- IV dose of edrophonium chloride - normally cholinesterase enzymes break down Ach but edrophonium blocks the enzymes - stops Ach breakdown and and inc Ach levels - relieves weakness temporarily
44
How is myasthenia gravis managed?
- reversible Ach inhibitors: pyridostigmine - immunosuppression - thymectomy - monoclonal Abs: rituximab
45
What is myasthenic crisis?
- complication causing acute worsening of symptoms - triggered by another illness e.g. resp tract - can lead to resp failure > ventilation - treatment with IVIG and plasma exchange
46
What is the pathophysiology of trigeminal neuralgia?
- can affect any combination of V1, V2 and V3 - 90% cases are unilateral - triggers: cold weather, spicy food, caffeine, citrus
47
What are the 3 branches of the trigeminal nerve?
- V1: ophthalmic - V2: maxillary - V3: mandibular
48
What is the presentation of trigeminal neuralgia?
- intense facial pain - comes on spontaneously, can last seconds to hours - electricity-like shooting pain
49
How is trigeminal neuralgia treated?
- carbamazepine
50
How do tension headaches present?
- mild ache across forehead in band like pattern - muscle ache in frontal, temporalis and occipitalis muscles - come on and resolve gradually: no visual changes
51
What are the causes of tension headaches?
- alcohol - depression - dehydration - stress - skipping meals
52
What are cluster headaches?
- severe and unbearable unilateral headaches - usually around the eye - crescendo pain which may affect temples
53
Who is the typical patient to suffer from cluster headaches?
- 30-50 y/o male smoker - attacks triggered by: alcohol, strong smells, exercise
54
What is the frequency of cluster headaches?
- attacks lasting 15 mins - 3hrs - may suffer multiple attacks per day for weeks or months - followed by pain free period lasting 1-2 years
55
What are the symptoms of cluster headaches?
- unilateral - red, swollen, watering eye - pupil constriction - ptosis - nasal discharge - facial sweating
56
What are the types of migraines?
- migraine with or without aura - silent migraine (with aura but without headache - hemiplegic migraine
57
What are migraine triggers?
- stress - bright lights - strong smells - dehydration - menstruation - abnormal sleep patterns - certain foods e.g. chocolate, cheese, caffeine
58
What are the symptoms of migraine?
- pounding/throbbing - usually unilateral - photophobia and phonophobia - nausea and vomiting
59
What is aura?
- visual changes - sparks in vision - blurring lines - lines across vision - loss of visual field
60
What is the treatment for migraine?
- paracetamol - triptans e.g. sumatriptan - NSAIDs - antiemetics
61
How do triptans work?
- 5HT receptor agonists (serotonin) - cause vasoconstriction in artery smooth muscle - inhibit peripheral pain receptors - reduce neuronal activity in CNS
62
What is prophylaxis for migraine?
- headache diary - propanolol, topiramate, amitriptyline - acupuncture - riboflavin
63
What is epilepsy?
- an umbrella term for a condition where there is a tendency to have seizures
64
What is a seizure?
- a transient episode of electrical activity due to abnormally excessive or synchronous neuronal activity within the brain
65
What are the causes of seizures?
- vascular - idiopathic - infection - trauma - dementia and drugs
66
What are some seizure triggers?
- fatigue - stress - alcohol and drugs - flashing lights - monthly periods - missing meals - fever
67
What is the pathophysiology behind epileptic seizures?
- normal balance between GABA and glutamate - balance shifts towards glutamate - more excitatory > inc glutamate stimulation and inc GABA inhibition
68
How is epilepsy diagnosed?
- electroencephalogram: electrical activity in brain - MRI brain
69
What is a generalised tonic-clonic seizure?
- loss of consciousness with muscle tensing (tonic) and muscle jerking (clonic) movements - tonic phase occurs before clonic - post-ictal period - limb contraction, extension, back arching and - usually last 2-3 minutes - ictal cry: sound resulting from chest contraction
70
What symptoms are experienced in the postictal period?
- amnesia - postictal nose wiping (ipsilateral) - confusion, irritability, feeling low - sore tongue from bitten
71
What is an absence seizure?
- commonly in school aged children - becomes blank and stares into space then abruptly returns to normal - unaware of their surroundings and unresponsive but still conscious - Episodes last 10-20 seconds and can disappear with age
72
What is the difference between tonic and atonic seizures?
- Tonic: person becomes stiff suddenly - Atonic: known as drop attacks where all muscles relax at once (lapse in muscle tone). These don’t tend to last for more than 3 minutes
73
What is a myoclonic seizure?
- sudden, brief muscle contractions like a jump - Seizures are brief but can occur in clusters, usually shortly after waking up - Patient remains conscious.
74
What is a complex partial seizure?
- consciousness may be impaired - Often occurs in the temporal lobe - May have post-ictal confusion
75
What is a focal seizure?
- only one part of the brain is affected - Can be aware or unaware - start in the temporal lobes and can affect hearing, speech, memory and emotions. - Presentation: hallucination, flashbacks, deja vu, doing things on autopilot.
76
What are the symptoms of focal aware (partial) temporal and frontal lobe seizures?
- Temporal: rising feeling in stomach, deja vu, unusual taste or smells, intense feelings of fear or joy - Frontal: ‘wave feeling’ going through head, stiffness or twitching in a limb
77
What are the symptoms of focal aware (partial) parietal and occipital lobe seizures?
- Parietal: numbness or tingling, arms or legs feel bigger or smaller than normal - Occipital: visual disturbance (coloured or flashing lights), hallucinations
78
How is epilepsy investigated?
- electroencephalogram (EEG) shows typical patterns - MRI brain
79
What is the treatment for epilepsy?
- sodium valproate - lamotrigine for child bearing aged women - carbamazepine: 1st line for focal seizure
80
How does sodium valproate work and what are the side effects?
- increases activity of GABA: has relaxing effect - inhibits sodium ion channels - teratogenic, liver damage, hair loss, tremor
81
What is an ischaemic stroke?
- 85% cases - a long TIA - caused by thrombosis/AF embolisation
82
What is a haemorrhagic stroke?
- 15% cases - ruptured blood vessel - caused by trauma, htn, berry aneurysm rupture
83
What are general symptoms of an anterior circulation stroke?
- hemiparesis - hemisensory loss - visual field defect (homonymous hemianopia withOUT macular sparing)
84
What are symptoms of an anterior circulation dominant hemisphere stroke?
- usually in left hemisphere - expressive and receptive dysphagia - dyslexia - dysgraphia
85
What are symptoms of an anterior circulation non-dominant hemisphere stroke?
- anosognosia - visuospatial dysfunction: geographical agnosia, dressing and constructional apraxia
86
What are symptoms of a posterior circulation stroke?
- often affects cerebellum + occipital lobe - clumsiness, difficulty walking in straight line - visual disturbance - slurred speech - headache, vomiting
87
What investigations are done for stroke?
- 1st line: CT head - gold: diffusion weighted MRI - blood test - carotid doppler
88
What is the management for stroke?
- aspirin 300mg stat and continued for 2 weeks - thrombolysis with alteplase (TPA) in 4.5 hr window - keep BP high to avoid reduced perfusion
89
What are the secondary prevention guidelines for stroke?
- Clopidogrel 75mg once daily - Atorvastatin 80mg started (not immediately) - Carotid endarterectomy or stenting - Treat modifiable risk factors
90
What is subarachnoid haemorrhage?
- bleeding into subarachnoid space between Pia mater and arachnoid membrane (where CSF is) - usually due to ruptured cerebral aneurysm
91
What are the symptoms of a subarachnoid haemorrhage?
- thunderclap headache described like being hit on the back of the head - neck stiffness - photophobia - visual changes - neurological symptoms
92
What are the causes of subarachnoid haemorrhage?
- cocaine use - sickle cell anaemia - connective tissue disorders - neurofibromatosis - autosomal dominant PKD
93
What is the presentation of brain tumours?
- varied dependent on tumour grade, site, type - headache - seizures - focal neurological symptoms - other non-focal symptoms e.g. cognitive problems or behavioural changes
94
What is the epidemiology of subarachnoid haemorrhage?
- black patients - female - age 45-70
95
What are risk factors for subarachnoid haemorrhage?
- htn - smoking - excess alcohol consumption - cocaine use - family history
96
How is a subarachnoid haemorrhage investigated?
- 1st line: NC CT head: hyperattenuation of blood in subarachnoid space - If negative: LP for CSF. Raised red cell count and xanthochromia (bilirubin) - If +ve: angiography
97
What is the management of subarachnoid haemorrhage?
- surgical intervention for aneurysms: endovascular coiling with catheter or clipping off - nimodipine: CCB that prevents vasospasm
98
What are the symptoms of a raised ICP headache?
- woken by headache - worse in the morning, lying down - exacerbated by coughing, sneezing, drowsiness - nausea and vomiting
99
What are symptoms of a brain tumour?
- raised ICP - Cushing's triad - focal neurology - epileptic seizures - lethargy + weight loss
100
What is Cushing's triad?
- bradycardia - irregular respiration - widened pulse pressure
101
What is the investigation for suspected brain tumour?
- MRI - biopsy - NO LP > contraindicated if high ICP
102
What are some types of primary brain tumour?
- astrocytoma - oligodendrocytoma - meningioma - Schwannoma
103
Which cancers commonly metastasise to the brain?
- lung - breast - renal cell carcinoma - melanoma
104
What are the types of gliomas?
- astrocytomas - oligodendroglioma - ependymoma - grade 1 are benign - grade 4 are most malignant: glioblastoma
105
What is the treatment for brain tumours?
- surgery: early resection - combined radiotherapy and chemotherapy
106
What is an acoustic neuroma?
- tumours of Schwann cells on auditory nerve - occur along cerebellopontine angle - symptoms: hearing loss, tinnitus, balance problems
107
What is papilloedema?
- swelling of optic disc 2º to raised ICP - blurring of optic disc margin - Elevated optic disc - Engorged retinal veins - Creases in the retina and haemorrhages around optic disc
108
What are red flag features of headaches?
- Constant - Nocturnal - Worse on waking - Worse on coughing, straining or bending forward - Vomiting
109
What is motor neurone disease?
- progressive, ultimately fatal condition - motor neurones stop functioning
110
What are the types of motor neurone disease?
- amyotrophic lateral sclerosis (ALS) - progressive bulbar palsy - progressive muscular atrophy - primary lateral sclerosis
111
What is the pathophysiology behind motor neurone disease?
- progressive degeneration of upper and lower motor neurones - sensory neurones spared
112
What are risk factors for motor neurone disease?
- genetic - smoking - SOD-1 mutation - exposure to heavy metals and pesticides
113
What is the presentation of motor neurone disease?
- progressive weakness of muscles affecting limbs, trunk, face, speech - weakness first noticed in upper limbs: fatigue when exercising - dysarthria - mixed LMN and UMN signs
114
What are signs of lower motor neurone disease?
- muscle wasting - reduced tone - fasciculations - reduced reflexes - Babinski -ve
115
What are the signs of upper motor neurone disease?
- increased tone or spasticity - brisk reflexes - no fasciculation - babinski +ve: upgoing plantar responses
116
What are the medications used for tremors?
- primidone - β blockers - gabapentin
117
What is the management of motor neurone disease?
- riluzole: sodium channel blocker - edaravone - non-invasive ventilation to support breathing at night
118
What is a transient ischaemic attack (TIA)?
- transient neurological dysfunction secondary to ischaemia without infarction - often precede a stroke - caused by carotid thrombo-emboli
119
What is the management of TIA?
- 300mg aspirin as soon as suspected - followed by clopidogrel
120
What is amaurosis fugax?
- sudden loss of vision in one eye: veiling - caused by infarct in retinal arteries - retinal branches from ophthalmic which branches from int carotid
121
What are the symptoms of a stroke in the anterior cerebral artery?
- weak, numb, contralateral leg
122
What are the symptoms of a stroke in the middle cerebral artery?
- weak, numb, contralateral side of the body - facial drooping - forehead sparing - dysphasia (temporal lobe)
123
What are the symptoms of a stroke in the posterior cerebral artery?
- visual loss - contralateral homonymous hemaniopia with macular sparing
124
What is the ABCD2 scoring system?
- risk of stroke following TIA - Age >60 (1) - BP > 140/90 (1) - Clinical symptoms: unilateral weakness (2), slurred speech, no weakness (1) - duration Sx: >1h (2). <1hr (1) - T2DM (1)
125
What are symptoms of meningitis?
- fever - photophobia - neck stiffness - non-blanching petechial rash - vomiting
126
What is Kernig's test?
- lie patient on back - flexing one hip and knee to 90 degrees and slowly straighten knee (keep the hip flexed) - spinal pain or resistance to movement in meningitis
127
What is Brudisinski's test?
- lie patient on back - gently lift head and neck and flex chin to chest - patient will involuntarily flex hips and knees
128
What is the management of meningitis?
1. Assess GCS 2. Blood cultures 3. Broad spectrum antibiotics 4. steroids e.g. dexamethasone
129
What antibiotics are given for meningitis?
- IV benzylpenicillin in primary care and immediate hospital referral - < 3mo: cefotaxime + amoxicillin - > 3mo: ceftriaxone
130
What special considerations should be made when treating meningitis?
- allergy to penicillin: if anaphylaxis switch to chloramphenicol - immunocompromised: potentially caused by listeria: add amoxicillin - recent travel: add vancomycin
131
What are contraindications for a lumbar puncture?
- abnormal clotting (platelets/coagulation) - petechial rash - raised ICP
132
What are differential diagnoses for meningitis?
- subarachnoid haemorrhage - migraine - flu and sinusitis - malaria
133
What is the public health response to meningitis?
- notify UK HSA - identify close contacts - PEP: ciprofloxacin or rifampicin for close contacts
134
What is meningitis?
- inflammation of the meninges (lining of the brain and spinal cord)
135
What are the causes of meningitis?
- infective: bacterial, viral, fungal, parasitic - non-infective: paraneoplastic, drugs, autoimmune
136
How does bacteria causing meningitis enter the body?
- extra cranial infection: nasal carriage, otitis media, sinusitis - via bloodstream: bacteraemic - neurosurgical complications: post op, infected shunts
137
What is meningococcal septicaemia?
- meningococcus bacterial infection in the bloodstream - causes the non blanching rash - infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages
138
Which bacteria commonly cause meningitis?
- Neisseria meningitidis (gram -ve diplococcus) - Strep pneumoniae (gram +ve cocci) - listeria monocytogenes (pregnancy) - group B strep in neonates
139
What are the most common causes of viral meningitis?
- HSV, enterovirus and VZV - CSF sample sent for PCR testing - treated with aciclovir
140
What are the possible complications of meningitis?
- hearing loss - cerebral palsy - seizures and epilepsy - cognitive impairment - disability
141
What is the definition and presentation of encephalitis?
- inflammation of the brain - flu-like illness - altered GCS, fever, seizures, memory loss
142
What are the causes of encephalitis?
- usually viral - herpes simplex - varicella zoster
143
What are the investigations for encephalitis?
- MRI head - LP: lymphocytic CSF and viral PCR
144
What is the management of encephalitis?
- supportive - aciclovir if HSV or VZV
145
What is cauda equina syndrome?
- nerve roots of cauda equina at bottom of spine are compressed - emergency
146
What is the anatomy of the cauda equina?
- collection of nerve roots travelling through spinal canal after cord terminates around L2/L3 - spinal cord tapers down into conus medullaris - nerve roots exit at vertebral level
147
What do the nerves of the cauda equina supply?
- sensation to lower limbs, perineum, bladder, rectum - motor innervation to lower limbs, anal and urethral sphincters - parasympathetic innervation of bladder and rectum
148
What is the aetiology of cauda equina syndrome?
- herniated disc (most common) - (metastasised) tumours - spondylolisthesis - abscess and trauma
149
What are signs of cauda equina syndrome?
- saddle anaesthesia - loss of sensation in bladder and rectum - faecal incontinence - bilateral sciatica and motor weakness
150
What is the management of cauda equina?
- emergency MRI and neurosurgical input to consider lumbar decompression surgery
151
What are the causes of spinal cord compression?
- degenerative disc lesions - degenerative vertebral lesions - TB - vertebral neoplasms - epidural abscess or haemorrhage
152
What is the presentation of spinal cord compression?
- sensory loss below level of compression - spastic paraparesis/tetraparesis - radicular pain at level of compression
153
Where is the sciatic nerve and what does it do?
- L4-S3 form sciatic nerve - supplies sensation to lateral lower leg and foot - motor for posterior thigh, lower leg and foot
154
What is sciatica?
- unilateral pain from the buttock radiating down the back of the thigh to below the knee or foot - causes: herniated disc, spondylolisthesis, spinal stenosis
155
What is the presentation of sciatica?
- electric or shooting pain - paraesthesia - numbness - motor weakness
156
What is dementia?
- progressive global decline of cognitive function without impairment of consciousness - mild cognitive impairment (MCI) is seen as a pre-cursor - typically affects temporal and parietal lobes
157
What is vascular dementia?
- results from many small infarcts - step-wise progression - infarcts affect function if damaging white matter
158
How can vascular dementia be prevented and which conditions is it associated with?
- aspirin or warfarin therapy - controlling BP - raised BP, past strokes
159
What is Lewy-body dementia?
- presence of Lewy bodies in the brainstem and neocortex - fluctuating cognitive impairment - hallucinations and Parkinsonism
160
What are the causes of peripheral neuropathy?
- Diabetes - Alcoholism - Vitamin (B12) deficiency - Infective/inherited - Drugs
161
What is the pathophysiology behind peripheral neuropathy (6 mechanisms)?
1. demyelination (Schwann cell damage) 2. axonal degeneration 3. nerve fibres cut or crushed 4. compression causing demyelination 5. infarction 6. infiltration by infection
162
What are the aetiologies of secondary intracerebral haemorrhages?
- clotting disorder - AV malformation - brain tumour - intracranial aneurysm - trauma
163
What are the classic cerebellar signs (DANISH)?
- D: dysdiadochokinesia - A: ataxia - N: nystagmus - I: intentional tremor - S: slurred speech - H: hypotonia
164
What is Charcot-Marie-Tooth disease?
- autosomal dominant disease affecting peripheral motor and sensory nerves - cause dysfunction in myelin and axons
165
What are classical presentations of Charcot-Marie-Tooth disease?
- high foot arches (pes cavus) - distal muscle wasting (stork calves) - lower leg and hand weakness - reduced tendon reflexes and sensory tone
166
What are the causes of peripheral neuropathy?
- Alcohol - B12 deficiency - Cancer and CKD - Diabetes and drugs (isoniazid, amiodarone and cisplatin) - Every vasculitis
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How is Duchenne's muscular dystrophy passed down and who does it affect?
- X-linked recessive mutation - boys affected exclusively
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What is the pathophysiology and presentation of Duchenne's muscular dystrophy?
- muscle is replaced with adipose tissue - causes difficulty getting up from lying down - skeletal deformities: scoliosis, hyperlordosis
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What is carpal tunnel syndrome?
- compression of the medial nerve as it travels through the wrist
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What is the anatomy of the carpal tunnel?
- between the carpal bones and flexor retinaculum - flexor retinaculum: runs across palmar side of wrist - median nerve and flexor tendons travel through
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Which muscles does the median nerve provide motor function to and which branch is it?
- abductor pollicis brevis - opponens pollicis - flexor pollicis brevis - palmar digital cutaneous branch
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What does the palmar cutaneous branch innervate?
- sensory to palm - thumb - index and middle finger - lateral half of ring finger
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What are the risk factors for carpal tunnel syndrome?
- repetitive strain - obesity - perimenopause - RA - diabetes
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How does carpal tunnel syndrome present?
- worse at night - sensory symptoms: numbness, paraesthesia, burning, pain - weakness of thumb movements, grip strength, difficulty with fine movement, wasting of thenar muscles
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What is Phalen's test?
- fully flexing the wrist and holding it there - wrists bent inwards at 90º - triggers numbness and parasthesia
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What is Tinel's test?
- tapping the wrist where the median nerve meets the carpal tunnel - triggers numbness and parasthesia
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What other investigations are done for carpal tunnel syndrome?
- nerve conduction studies - carpal tunnel questionnaire
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How is carpal tunnel syndrome managed?
- rest and altered activities - wrist splints - steroid injections - surgery: flexor retinaculum cut to relieve pressure
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What occurs in the frontal lobe?
- voluntary and planned motor behaviours - motor speech area (Broca's) - personality - planning
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What is the function of the temporal lobe?
- hearing - language comprehension - semantic knowledge - memory - emotional behaviour
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What is Alzheimer's disease?
- leading cause of dementia - progressive neurodegenerative disorder causing deterioration in mental performance - general atrophy of brain - frontal and temporal lobes affected in particular
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What is the presentation of Alzheimer's?
- temporal: episodic memory disorder - parietal: visuospatial difficulties - receptive and expressive dysphagia - emotional disorder/psychosis - problems with planning and problem solving - early loss of language (subtle)
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What is the pathophysiology of Alzheimer's disease?
- accumulation of β-amyloid peptides > plaques - degrades amyloid precursor protein - leads to neuronal damage, neurofibrillary tangles, amyloid plaques - loss of Ach
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Which areas of the brain are most affected by Alzheimer's?
- hippocampus - amygdala - temporal neocortex - subcortical nuclei
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What are the risk factors for Alzheimer's?
- 1st degree relative - Down's - depression/loneliness - decreased exercise, physical activity
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What are β-amyloid plaques?
- excess deposition of β-amyloid - amyloid precursor protein broken down (found in cell membrane of neurones) - accumulate between synapses and affect nerve transmission - cause localised inflammation
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What is the management of dementia?
- AChE inhibitors: donepezil: inc cholinergic transmission in brain - NMDA antagonists: inhibits glutamate receptors - antipsychotics
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What is fronto-temporal dementia?
- frontal and temporal lobe atrophy: loss of spindle neurones - behaviour change - disinhibition and emotional unconcern
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How is dementia investigated?
- CT/MRI to look for lesions/atrophy - bloods - questionnaires: 6 CIT
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What is syncope?
- temporarily losing consciousness - due to disruption of blood flow to brain - also called vasovagal episodes or fainting
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What is the presentation of syncope?
- hot and clammy, sweaty - heavy - dizzy, lightheaded - vision going dark
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What are the primary causes of syncope?
- dehydration - missed meals - extended standing - vasovagal response to stimuli: surprise, pain
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What are the secondary causes of syncope?
- hypoglycaemia - dehydration - anaemia - infection - anaphylaxis - arrhythmia
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What investigations are done for syncope?
- ECG/24 hr ECG - echocardiogram - bloods: FBC, electrolytes, blood glucose
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What are some causes of lower motor neurone injury?
- MND, spinal muscular atrophy, polio - Guillain Barre - neuropathies - myasthenia gravis - myositis
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What is the presentation of spinal muscular atrophy?
- symmetrical, proximal muscle weakness caused by loss of motor neurons - lower limbs more affected than upper - affects bulbar function and breathing
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Describe SMA 1 and 2
- SMA 1: onset in first few months, death within 2 years - SMA 2: onset in 18 months, never walk but survive to adulthood
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Describe SMA 3 and 4
- SMA 3: onset after 1y/o, walk but later lose ability, resp affected - SMA 4: onset in 20s, ability to walk for short distances, everyday tasks > fatigue. resp + life expectancy not affected
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What is the pathophysiology behind neuropathies?
- primary demyelination > secondary axonal degeneration - primary axonal degeneration > secondary demyelination
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What are the types of peripheral neuropathies?
- mononeuropathy: one nerve - mononeuropathy multiplex: several nerves, no pattern - polyneuropathy: many nerves (distal + symmetrical)
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What is Lambert Eaton syndrome?
- autoimmunity against presynaptic Ca channels in NMJ - symptoms improve with exertion - associated with small cell lung carcinoma - symptoms start with extremities
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What is the presentation of Lambert Eaton syndrome?
- proximal muscle weakness - diplopia - ptosis - dysphagia
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What is the treatment of Lambert Eaton syndrome?
- Amifampridine - immunosuppressants: prednisolone
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How can you differentiate between UMN and LMN lesions?
- forehead spared in UMN - ask patient to raise eyebrows - if can move both sides then UMN lesion - if one side affected then LMN lesion
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What is the presentation of a radial nerve palsy and what are the nerve roots?
- roots C5-T1 - wrist drop - innervates extensor muscles
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What is the presentation of a ulnar nerve palsy and what are the nerve roots?
- roots C8 + T1 - claw hand (4th and 5th fingers)
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What are differential diagnoses for epilepsy?
- syncope - cardiac arrhythmia - panic attack - non-epileptic + dissociative seizures - TIA - migraine
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What is Brown-Sequard syndrome?
- hemisection of the spinal cord - involves anterolateral system and DCML pathway - symptoms occur below the lesion
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What are the symptoms of Brown-Sequard?
- contralateral loss of pain and temperature - ipsilateral loss of proprioception and vibration - ipsilateral UMN weakness below lesion
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Describe GCS?
- Eyes, verbal response, motor response - max score is 15, min is 3 - 8/15 or below: secure airway