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6. Nervous (Neuro & Psych) > Clinical Neurology > Flashcards

Clinical Neurology Flashcards

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1
Q

Describe the clinical spectrum of pathological MND.

A
  • UMN disease
  • PLS [primary lateral sclerosis]
  • PBP [progressive bulbar palsy]
  • ALS [amyotrophic lateral sclerosis]
  • PMA [progressive muscular atrophy]
  • LMN disease
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2
Q

Describe the clinical features seen in MND.

A
  • more UMN: increased tone, hyperreflexia, extensor-plantar response, spastic gait, exaggerated jaw jerk, slowed movement
  • ‘neutral’ symptoms: speech, swallow, speaking symptoms
  • more LMN: wasting, weakness, fasciculations, reduced/absent reflexes
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3
Q

Describe the investigations and management regarding MND [4].

A
  • El Escorial criteria
  • neuroimaging and lab studies are required to exclude other disease; MND is a diagnosis of exclusion
  • ‘general’ Mx: speech therapy, ‘voice banking’, dietician support, gastrostomy, respiratory care, riluzole (only licenced Dx)
  • symptomatic management for sialorrhoea, muscle cramp, muscle spasm, respiratory, dyspnoea and anxiety
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4
Q

Describe tremor and the conditions in which it may occur [5].

A
  • rhythmic sinusoidal oscillation of a body part
  • essential tremor: most common postural tremor when hand is outstretched; slow progression, but may be disabling
  • Wilson’s disease
  • asterixis (hepatic encephalopathy)
  • titubation (oscillations of the head)
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5
Q

Describe dystonia [3].

A
  • sustained or intermittent muscle contractions causing abnormal, often repetitive, postures / movements or both
  • typically patterned, twisting, and tremulous
  • often initiated by a voluntary action; may be improved by a sensory tic
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6
Q

Define chorea and ballism [2], and name the main causes [5].

A
  • chorea: brief, purposeless movements that flit and flow from one body part to another; patients often appear restless or fidgety
  • ballism: extreme variant of chorea, involving proximal joints and resulting in large amplitude flinging movements, often in a hemi-body distribution
  • causes: BG lesions, Sydenham chorea, Huntington chorea, APLS, neuroacanthocytosis
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7
Q

Describe myoclonus and negative myoclonus.

A
  • brief, electric-shock like jerks, caused by brief activation of a muscle group, leading to a jerk of an affected body joint
  • negative myoclonus: produced by temporary cessation of muscle activity (e.g., liver flap)
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8
Q

Describe tics.

A
  • repetitive, stereotyped movements / vocalisations; these are initially suppressable
  • anxiety and discomfort leading up to tics causes a buildup and flurry of tics when allowed to relax
  • motor tics include blinks, head jerks, arm/leg jerks, complex sequence jerks
  • Gilles de la Tourette’s syndrome: persistent, multiple motor and vocal tics, often associated with psychiatric disturbance
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9
Q

[1/3] Describe the epidemiology (risk factors, genes, protective factors) and pathology of Alzheimer’s disease.

A
  • risks: male, pesticides, prior head injury, rural living (well-water drinking), beta blockers, agriculture
  • genes: GBA, LRRK2, PARKIN, SCNA
  • protective: tobacco, coffee, NSAIDs, CCBs, alcohol
  • pathology: degeneration of the substantia nigra and loss of the dark pigment in the SN locus coeruleus. Lewy bodies are present, which contain alpha-synuclein
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10
Q

[2/3] Describe the motor and non-motor presentations of Alzheimer disease [3 + 4].

A
  • motor: TRAP (tremor, rigidity, akinesia, posture)
    • tremor: pill-rolling
    • rigidity: cog-wheel and lead pipe. rigidity felt throughout movement. Froment’s test is +ve
    • akinesia: slow alternating repetitive movements
    • posture: stooped, slow turning, small shuffling steps
  • non-motor (psych): dementia, depression, psychosis, REM sleep behaviour
  • non-motor (other): constipation, GI motility, orthostatic hypotension, sialorrhoea
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11
Q

[3/3] Describe the diagnosis and management options for Alzheimer’s; this includes symptomatic management [4 + 3].

A
  • clinical diagnosis: akinesia + one of the other symptoms (TRAP)
  • diagnostic testing is not normally needed; brain imaging (+ SPECT) can show reduction of the substantia nigra from a ‘comma’ to a ‘full stop’.
  • dopaminergic Tx (L-DOPA, MAOB inhibitors, COMT inhibitors, amantadine) should be initiated when symptoms are disabling / uncomfortable
  • symptomatic treatments:
    • dementia: AChI, rivastigmine
    • depression, psychosis (SSRIs, TCAs, antipsychotics)
    • sleep disturbance (BZDs, melatonin)
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12
Q

Describe the indications for neuroimaging, and the differences in CT and MRI.

A
  • headache/raised ICP, seizure, weakness, stroke, trauma, LOC, neurological deficit, post-op
  • CT: primary modality used. excellent bony detail and spatialities. Acquisition is not direct but instead axial
  • MRI: best for soft tissue. Not compatible with pacemakers, implants, and ICU equipment
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13
Q

Describe the stages of MRI.

A
  • T1 hyperdense: shows fat + 4Ms (methemoglobin - subacute haematoma), minerals (Ca, Mg), melanin (melanoma), mush (proteinous fluid)
  • T1 hypointense: water, cortical bone, arteries
  • T2 hyperintense: fat, water (‘T2 = H2O’), air, fluids, oedema, demyelination, gliosis, some tumours
  • T2 hypointense: blood products, minerals, air, cortical bone, arteries
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14
Q

Describe the general principles of neuromuscular disorders, based on which part of the NMJ they affect.

A
  • presynaptic: intially, fatigue improves with exercise. autonomic features are common. ocular muscles are rarely involved.
  • postsynaptic: fatigues with exercise. autonomic features tend not to occur. ocular features (e.g., ptosis, diplopia) are common.
  • muscle: myalgia, muscle weakness, wasting, hyporeflexia, myotonia etc.
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15
Q

Describe where in the NMJ the three main NMJ pathologies (botulism, LEMS, MG) occur, and therefore what their core clinical features are.

A
  • LEMS -> presynaptic calcium channels (autoantibodies to, closely related to SCLC). presynaptic -> proximal weakness initially improving with exercise, autonomic features (dry eyes/mouth, orthostatic hypotension, constipation, ED, reduced reflexes)
  • botulism -> presynaptic protein cleaving, blocking vesicle blocking with the presynaptic membrane. features have rapid onset, similar to LEMS
  • MG -> postsynaptic ACh receptors (autoantibodies to, closely related to thymic hyperplasia). postsynaptic -> muscle features (weakness, dysphagia, larynx / jaw/ neck) weakness, ocular features (ptosis, diplopia)
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16
Q

Name the five main categories of muscle pathology, and give examples of each.

A
  • immune: dermatomysitis, polymyositis
  • inherited: muscular dystrophy, dystrophinopathies, limb girdle muscle dystrophy, myotonic dystrophy
  • congenital: myasthenic syndromes, myopathies
  • infective: coxsacchie, trypanosomiasis, borrella etc.
  • rhabdomyolysis: crush injury, AKI
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17
Q

Describe and define cognition and dementia.

A
  • cognition: the mental action of acquiring knowledge and understanding through thought, experience, and senses. it comprises attention, social and executive function, memory, and language
  • dementia: undoing of the mind. requires evidence of significant cognitive decline, interference with independence, and the condition not to be better explained by another condition (and not occur exclusively in the setting of delirium).
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18
Q

Describe the main acute [5] causes of dementia.

A
  • viral encephalitis of the temporal lobe (focal injury)
  • head injury of the frontal lobe (focal injury)
  • stroke (focal injury - presentation depends on area involved)
  • transient global amnesia: anterograde > retrograde memory loss (difficulty ‘laying down’ memory) for <24h
  • transient epileptic amnesia: recurrent TGA; carries out complex activities with no recollection; responds to AEDs
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19
Q

Describe the main subacute [4] causes of dementia.

A
  • VINDICATE: infection (HIV, syphilis); degenerative (CJD, below); intoxication (alcohol, CO); autoimmune (limbic encephalitis, below)
  • functional/subjective cognitive impairment: everyday forgetfulness which impacts on function
  • Creutzfeld-Jakob disease: degenerative proteinopathy. May be sporadic, variant, iatrogenic, or genetic; all forms terminate in spongiform change in the brain
  • limbic encephalitis: antibody mediated (VCKC; anti-Hu) causes short-term memory deficit
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20
Q

Describe the pathology of Alzheimer’s, as it relates to dementia.

A
  • Alzheimer’s forms, solely or in part, 75% of dementias.
  • neurodegenerative proteinopathy (amyloid) disrupts cholinergic pathways, causing synaptic loss, then extracellular plaques, and intracellular neurofibrillary tangles.
  • degeneration of the medial hippocampus (and later, parietal lobes) causes general forgetfulness, apraxia, and visuo-spatial difficulties
  • temporoparietal atrophy, decreased uptake on SPECT, and increased tau protein
  • atypical presentations more associated with younger patients, including posterior cortical atrophy (visuospatial), and progressive primary aphasia (semantic, logopenic, non-fluent naming / repeating)
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21
Q

Name and describe the main (non-Alzheimer) causes of gradual-onset dementia, along with their management [5]. Hint: most can be summarised as dementia, plus another core clinical feature.

A
  • frontotemporal dementia (FTD): dementia, psychiatric (disinhibition, apathy, compulsion, loss of insight). trial trazodone and anti-psychotics
  • vascular dementia (VaD): dementia with cerebrovascular disease (decreased attention, slowed processing, executive factors). manage vascular factors and trial cholinesterase inhibitors
  • dementia with Lewy bodies (DLB): dementia with motor features (fluctuating cognition, visual hallucinations, extrapyramidal features). Give levodopa and small-dose anticholinesterase inhibitor.
  • Parkinson’s dementia: overlaps with Parkinson’s (!!)
  • Huntington’s: dementia of early onset (30-50) with psychiatric symptoms (mood/personality change, chorea, psychosis)
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22
Q

Describe the key clinical features of CNS tumours.

A
  • progressive neuro deficits, motor weakness, headache, seizure
  • balance problems and morning headache/N&V (due to posterior fossa location)
  • papilloedema
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23
Q

Name the four main types of nervous system tumour, and give a brief overview of their classifications.

A
  • ASTROCYTOMA (60%)
    • I. truly benign, surgery curative
    • II. low grade, all will dedifferentiate if not treated
    • III. anaplastic astrocytoma
    • IV. glioblastoma multiforme, spreads by white matter and dismal prognosis. treated by the Stupp protocol
  • OLIGODENDROCTOMA (20%). usually affects frontal lobes, and calcifies (unlike astrocytoma)
  • MENINGIOMA
    • classification: classic, atypical, malignant. surgery is curative
  • NERVE SHEATH TUMOURS
    • schwannoma, suggests NF II
    • pineal gland tumours
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24
Q

For what is the Stupp protocol is used, and what it is comprised of? [4]

A
  • the Stupp protocol is used for grade IV astrocytoma (glioblastoma multiforme, GBM).
  • it comprises surgery, radiotherapy, and temozolmide.
  • carmustine wafers may be used as chemotherapy in the brain
  • inform the DVLA in all cases
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25
Q

Describe the Simpson’s grading of resection of surgery.

A
  • I. complete removal + bone + dura (best)
  • II. complete removal + coagulation of dura
  • III. complete removal, without coagulation
  • IV. subtotal resection
  • V. simple decompression without biopsy (worst)
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26
Q

Name the normal components of the skull (and their proportions), along with the Monroe-Kellie doctrine.

A
  • brain (80-85%): ICF, tissue, ECF
  • blood (5-8%)
  • CSF (8-12%)
  • Monroe-Kellie: compensatory mechanism for expanding masses; when present, these will push other components outward (e.g., via the foramen magnum)
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27
Q

Brain ICP physiology:

  • give the formulae for cerebral perfusion pressure, and cerebral blood flow
  • what is the normal ICP? which chemicals may cause brain vessel dilation?
  • at what ICP does autoregulation fail?
A
  • CPP = MAP - ICP
  • CBF = CPP / CVR [cerebrovascular resistance]
  • normal ICP = 7-15mmHg
  • autoregulation decompensates at 150mmHg
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28
Q

Name the causes [5] and clinical features [2] of raised ICP.

A

CAUSES
- mass effect (tumour, infarct, contusion, haematoma, abscess)
- swelling (ischaemia, acute liver failure)
- increased CVP (venous sinus thrombosis, CHF, IJV obstruction)
- increased CSF production (choroid plexus papilloma)
- communicating hydrocephalus (SAH, meningitis, malignancy)
FEATURES
- early: reduced LOC, headache, papilloedema, change in vision, N&V
- late: coma, fixed/dilated pupils, hemiplegia, bradycardia (CUSHING TRIAD), hyperthermia, increased urinary output

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29
Q

Describe the management of raised ICP/hydrocephalus [4].

A
  • maintain CPP to prevent ischaemia
  • maintain head in midline, loosen tube-ties, collars, avoid coughing/gagging etc., elevate head of bed to 30-45deg, decrease stimuli (noise, light etc.)
  • use diuretics (mannitol, hypertonic saline, furosemide, urea)
  • barbiturate coma (nuclear option): allows decompression, removal of mass, and/or diversion of CSF
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30
Q

Describe the main features and management of idiopathic intracranial hypertension (IIH) [2].

A
  • women of childbearing age; headache, tinnitus, radicular pain, risk of permanent visual loss (precursors -> double vision, visual burning, papilloedma)
  • weight loss, carboanhydrase inhibitors (e.g. acetazolamide), diuretics, CSF shunts, interventional radiology
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31
Q

Define the term traumatic brain injury (TBI) and give the main risk factors.

A
  • a nondegenerative, non-congenital insult to the brain from an external mechanical force, possibly leading to impairment of cognitive, physical, or psychosocial function.
  • male, young, elderly, previous head injury, urban dwelling, alcohol/drugs, low income, falls, assaults, anticoagulants etc.
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32
Q

Describe the management (including the GCS classification) of traumatic brain injury [6 + 3].

A
  • most deaths occur within 1hr (primary); the secondary peak occurs after 6-8hr due to hypoxia; these deaths are potentially preventable.
  • manage ABCDE with C-spine control
  • GCS consists of
    • eye opening (4-1)
    • verbal (5-1)
    • motor (6-1)
  • patients with risk factors (GCS <13 initially. <15 after 2hr, skull fracture, seizure, focal neuro deficit, vomiting, suspected NAI) should have CT
  • consider AEDs to prevent seizure
  • good nutrition and avoidance of steroids
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33
Q

Describe the four main types of head injury.

A
  • sudural haematoma: banana shape, crosses sutures; Mx with craniotomy or Burr holes (if chronic and calcifies)
  • epidural haematoma: concave, lemon shape, does not cross sutures
  • intracerebral haemorrhage: bleeding within brain parenchyma
  • diffuse axonal injury: localised injury due to shearing factors, occurs at grey-white interface
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34
Q

Describe the aims of neurosurgery in relation to traumatic brain injury [4].

A
  • prevent secondary injury (hypoxia, hypotension, etc.)
  • remove haematoma, coagulate sites of bleeding, clearing the brain
  • increasing venous drainage, drop ICP, maintain CPP
  • can reduce ICP in the case of medical Mx failure
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35
Q

Describe the key features of brainstem death [3 + 5].

A
  • brainstem loses function despite intact cardiovascular function
  • exclude drugs (e.g. anaesthesia), hypothermia, and severe metabolic/endocrine disturbance
  • 2x CN tests must be performed by 2 doctors
    • II, III: pupil response
    • V, VII: corneal reflex
    • III, VI, VIII: vestibulocular reflex
    • IX, X: gag reflex
    • apnoea test: respiration
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36
Q

Name the red flags associated with back pain [7].

A

worrying pathologies include cancer, infection, fracture, cauda equina syndrome, and AAA

  • failure to improve after 4-6 weeks of conservative treatment
  • night pain or pain at rest
  • cancer (>50, unintended weight loss, previous cancer)
  • infection (fever, chills, immunosuppression, IV drug abuse, dental status, foreign travel)
  • fracture (>50, osteoporosis, trauma, chronic steroid use)
  • cauda equina (bilateral pain, incontinence, leg weakness, decreased anal tone, loss of perineal sensation)
  • AAA (>60, pulsatile mass, pain at rest)
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37
Q

Describe the motor weakness, screening exam, and change in reflexes associated with the main lower limb neuropathies (L4, L5, S1).

A
  • L4: weak quadriceps extension; screen with squat and rise; decreased knee jerk
  • L5: weak dorsiflexion of the great toe and foot; screening by heel walking; no associated reflex change
  • S1: weak plantarflexion of the great toe and foot; screening by toe walking; decreased ankle jerk
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38
Q

Describe the key investigations and management of lower back pain and sciatica.

A
  • investigations only undertaken with red flags
  • 1st line MRI; CT if contraindicated; XR to exclude AS (younger) or vertebral collapse (elderly)
  • lab tests: tumour markers (inc. PSA), monoclonal bands, WCC/ESR, ALP / Ca / PO4, HLA-B27
  • explanation and reassurance, exercise, NSAIDs/paracetamol -> opioids, physiotherapy
  • refer if pain intractable, or with suspicion of serious pathology
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39
Q

Name the three main portions of the spinal cord that relate to motor symptoms, and how they affect patients (e.g., unilateral or bilateral).

A
  • CST (corticospinal tract) = ipsilateral
  • dorsal columns = ipsilateral
  • STT (spinothalamic tract) = contralateral
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40
Q

What are the main features of UMN and LMN lesions?

A
  • UMN: increased tone, no fasciculation, no marked wasting, hyperreflexia
  • LMN: decreased tone, wasting, fasciculation, diminished reflexes
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41
Q

Name the four main spinal cord compression syndromes, including
their distribution within the cord.

A
  • central cord compression: central cord
  • anterior cord: anterior cord, sparing dorsal columns
  • Brown-Sequard syndrome: half of cord (L / R)
  • cord transection: whole cord
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42
Q

Name and describe the five types of peripheral neuropathy (hint: easier to think of anatomy from spinal cord to muscle).

A
  • ganglionopathy: isolated sensory dysfunction (seen in Sjogren’s, SCLC, platins, vitamin B6 tox)
  • radiculopathy: pain radiates along root distribution (seen in disc prolapse, infection CMV/HSV/syphilis, GBS)
  • plexopathy (traumatic injury, birth, malignancy)
  • peripheral neuropathy (mononeuropathy, mononeuritis multiplex, length dependent
  • alpha-motor neurone disease (MND)
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43
Q

Describe the plexopathies associated with the upper limb [4].

A
  • Erb-Duchenne: shoulder is depressed, increasing traction on the upper plexus.
    • motor cycle accident, birth canal trauma
    • upper arm weakness, hand sparing
  • Klumpke palsy, associated with stretching of axilla
    • caught in a machine, falls from height and holds on by upper arm
    • paralysis of hand, but arm spared
  • Pancoast tumour -> Horner syndrome
  • Parsonage-Turner plexopathy: inflammatory proximal plexopathy after physiological stress (inc. infection, trauma etc.)
    • severe axillary / shoulder pain, spontaneous recovery
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44
Q

Name the causes of lower limb radiculopathy [4].

A
  • foraminal stenosis
  • disc herniation
  • lumbar canal stenosis
  • cauda equina, conus medullaris syndromes
45
Q

Describe the presentations of lower limb mononeuropathy.

A
  • femoral: weak hip flexion, knee extension, lost patellar reflex. hip adduction is spared.
  • obturator: weakness of hip adduction
  • sciatic: weakness of knee flexion, foot movements
  • perOneal: rare in isolation. brings foot up and Out. DEep peroneal: Dorsiflexion and Extension
46
Q

Describe the inheritance pattern of Duchenne muscular dystrophy.

A
  • x-linked recessive

- dystrophin gene, connects actin filaments to membrane

47
Q

Describe the inheritance of Huntington’s.

A
  • autosomal dominant
  • trinucleotide repeat [CAG -> glutamine] on huntingtin gene, chromosome 4
  • amount of glutamine doubled (20->42)
48
Q

Describe the inheritance of spinal muscular atrophy (SMA).

A
  • SMN1 produces 100% functional SMN protein
  • SMN2 produces 10% functional SMN protein
  • autosomal recessive, SMA affects SMN1 and causes only 10% functional SMN2
49
Q

Describe the inheritance of Kennedy’s disease.

A
  • X-linked

- affects androgen receptor (therefore gynaecomastia and infertility can present)

50
Q

Name the genes that can contribute to Alzheimer’s.

A
  • APP chromosome 21 (Down syndrome)
  • presenilin 1 chr 14
  • presenilin 2 chr 1
51
Q

Describe the pathology and epidemiology of multiple sclerosis.

A
  • autoimmune demyelination of the axons in the CNS (oilgodendrocytes)
  • areas of inflammation (plaques) are disseminated in time and space
  • more common further from the equator (vitamin D deficiency)
  • typically presents in 30s-40s, female : male 3:1
52
Q

Describe the clinical courses of MS.

A
  • primary relapsing-remitting: episodes of inflammation, but baseline function returns
  • progressive: function gradually worsens
  • progressive MS may be secondary to relapsing-remitting, where function returns but then gradually does not
53
Q

Describe the clinical features of MS, as they relate to their anatomical areas of inflammation.

A
  • pyramidal: increased tone, spasticity, weakness; extensors [upper]/flexors [lower]
  • brainstem: depends on location; e.g. diplopia CN VI, facial weakness CN VII
  • sensory: pain, paraesthesia, loss of proprioception / vibration sense, numbness, trigeminal neuralgia
  • optic: optic neuritis 1-2 weeks
  • cerebellar: dysarthria, ataxia, nystagmus, intention tremor, past pointing, dysdiadokinesis
  • LUTS
54
Q

What are Uthoff’s and L’hermitte’s signs?

A
  • Uthoff: recurrence / emergence of symptoms with heat
  • L’hermitte’s: electrical sensation down spine with forward flexion of neck
  • seen in MS
55
Q

Describe the radiological findings seen in MS.

A
  • small ovoid T2/FLAIR hyperintensities perpendicular to lateral ventricles and corpus callosum
  • Dawson’s fingers in the sagittal plane
  • ‘open ring’ (gadolinium constrast)
  • T1 hypointensities at sites of prior demyelination
  • lesions are small and peripheral (unlike neuromyelitis optica, where lesions are longitudinally extensive)
56
Q

Describe the investigation and defined syndromes of MS.

A
  • clinically isolated syndrome (CIS): first demyelinating event
  • radiologically isolated syndrome (incidental finding, 1/3 develop MS)
  • imaging should be undertaken
  • if imaging does not reveal abnormalities, but clinical suspicion is high, look for ancillary evidence:
    • oligoclonal bands in the CSF (intrathecal IgG synthesis)
    • visual evoked potentials (VEPs)
    • OCT; can indicate prior optic neuritis
57
Q

Describe the management options for acute episodes of MS.

A
  • spasticity: antispasmodics, physio, baclofen, tizanidine, botox, cannabis
  • sensory: gabapentin, amitriptyline, TENS, acupuncture, lignocaine
  • LUTS: bladder drill, oxybutynin, desmopressin, catheter
  • fatigue: amantadine, modafinil, hyperbaric O2
58
Q

Describe the disease modifying therapy options for MS [4].

A
  • 1st line: interferon beta, glatiramer acetate, tecfidera, aubagio
  • 2nd line: monoclonal antibodies (prevents lymphocytes crossing BBB), fingolimod, cladribine, natarizumab (risk of PML, screen serum JC virus)
  • 3rd line: mitoxantrone (cardiac toxicity, chemotherapy), HSCT
  • single agent only
59
Q

Describe the pathology and management of neuromyelitis optica (NMO) [4].

A
  • NMO-IgG is directed against aquaporin-4
  • 3+ spinal segments affected
  • 1st line: steroids, plasma exchange, cyclophosphamide
  • 2nd line: rituximab, AZA, MYP mofetil
60
Q

Describe acute disseminated encephalomyelitis (ADEM) [5].

A
  • CNS analogue to GBS
  • acute reaction to recent infection or vaccination
  • presents with multifocal neuro deficits and/or encephalopathy
  • incomplete T2 hyperintensities forming and incomplete ring
  • IV steroids, IVIg, plasma exchange; most recover entirely
61
Q

Describe the clinical features, associated conditions, and management of optic neuritis [4].

A
  • painful unilateral visual loss, worse on movement
  • reduced acuity, colour vision, RAPD +ve, optic nerve enhancement on imaging
  • occurs in NMO, sarcoidosis, Bartonella, syphilis, paraneoplastic syndromes (antibody against CRMP-5)
  • most recover in 2-4wks. IV steroids can help acutely but does not affect long term outcome
62
Q

Name the complications associated with untreated CNS infection [2].

A
  • herniation, cord compression, necrosis, paralysis, death

- chronic: hearing loss, epilepsy, cognitive impairment, hydrocephalus, limb loss, blindness, CP, quadriplegia etc.

63
Q

Name the symptoms seen in CNS infection, and define encephalitis and meningoencephalitis. Give also the two key signs observed on clinical examination [5].

A
  • symptoms: headache, vomiting, pyrexia, neck stiffness, photophobia, lethargy, confusion, rash, purpuric rash with N meningitidis
  • encephalitis: mental status change, confusion, obtundation, coma, behaviour/speech disturbance
  • meningoencephalitis: features of both
  • [K][e]rnig sign: unable to [k]nee [e]xtend
  • Brudzinski sign: patient flexes hip and knee with head flexion
64
Q

Describe how suspected CNS infection should be investigated.

A
  • perform LP if clinically feasible, UNLESS
  • immunocompromised, Hx of CNS disease, new onset seizure, papilloedema, abnormal LOC, focal neuro deficit: give CT > LP
  • take 4 samples
      1. haematology (cell count, lymphs v neuts)
      1. microbiology (gm stain, culture)
      1. chemistry (glucosa, protein)
      1. haematology (repeat)
65
Q

Describe the CSF interpretation of CNS infection type (bacterial, viral, fungal, TB).

A
  • bacterial: protein 100-1000, <40% glucose, 100-10,000 WBCs (N > L)
  • viral: protein 10-100, normal glucose, 100-1,000 WBCs (L > N). consider PCR and VZV Ig
  • fungal: protein 100-500, decreased glucose, 100-1,000 WBCs (L > N); consider cryptococcal antigen
  • TB: protein 100-1,000, reduced glucose, 100-500 WBCs (L > N)
66
Q

Describe the management of CNS infection [3; 1+6, 2+3; 3+0]

A
  • not allergic, <60
    • cefotaxime 2g QDS, or ceftriaxone 2g BD
    • dexamethasone 10mg QDS
    • BOTH should be taken
    • if >60, + amoxicillin 2g IV 4-hourly
    • if pneumococcal resistance is suspected, add vancomycin 15-20mg/kg BD and rifampicin 600mg BD
    • if HSV suspected due to encephalitis, + acyclovir
  • allergic, <60
    • chloramphenicol 25mg/kg +
    • dexamethasone 10mg QDS
    • > 60: add co-trimoxazole 10-20mg/kg
  • antibiotics must be administed IV. do not delay abx for CSF results.
67
Q

Describe the public health management of CNS infection.

A
  • contact prophylaxis: droplet precaution, face masks/coverings
  • rifampicin 600mg 12hrly 4 doses (reduced efficency COC, red urine, contact lens staining)
  • ciprofloxacin oral 500mg oral single dose, ceftriaxone IM 250mg single dose
68
Q

Name and describe the main bacteria that can infect the CNS tract [4].

A
  • s pneumoniae: commonly found in nasopharynx, can infiltrate in BOS#, DM, alcoholism, cochlear implants etc.
  • l monocytogenes: resistant to ceftriaxone (req. ampicillin / amoxicillin)
  • n meningitidis
  • E coli
69
Q

Name the non-bacterial pathogens that may infect the CNS tract.

A
  • cryptococcus (HIV CD4+ <100)

- HSV, VZV, CMV, enteroviruses, arboviruses, HIV

70
Q

Describe the differential diagnosis of pathogen in CNS infection, based on age.

A
  • neonates (LESs than one month): Listeria, E coli, S agalactiae [note: h influenzae cases dropped due to vaccine]
  • 10-65: N meningitidis, s pneumoniae
  • > 65: Listeria, s pneumoniae
71
Q

Name the function and types of neurology AHPs.

A
  • improve function, reduce symptoms/burden, enable partial or full independence, optimise wellness and QoL etc.
  • OT, physiotherapy, SALT, dietician, orthotist, music therapist
72
Q

Define epilepsy and give the excluders [6].

A
  • a tendency to recurrent, spontaneous epileptic seizures. cannot be epilepsy if there is a clear provoking (acute, reversible) cause.
  • trauma (stroke, haemorrhage, meningitis etc.)
  • metabolic causes
  • medications (bupropion, tramadol, fluoroquinolones, cephalosporins, carbapenems)
  • alcohol, cocaine
  • systemic infection, renal failure
73
Q

What are the main differences between syncope and seizure? [5]

A

seizure is more likely if:

  • sustained tonic-clonic activity
  • tongue biting
  • urinary / faecal incontinence
  • post-ictal state
  • preceding aura
74
Q

Describe the key aspects of history taking in seizures.

A
  • risk factors: abnormal birth / gestation, previous seizures (e.g., febrile), head injury, stroke, infection etc.
  • provoking factors (card 72)
  • driving and occupation
  • neuro deficits indicating a focal lesion
75
Q

Excluding imaging, name and describe the investigations relating to epilepsy [4]

A
  • lab evaluations (electrolytes, tox screen)
  • ECG for long QT
  • CP if concerns re infection
  • EEG (neither sensitive nor specific)
76
Q

Describe the imaging findings in epilepsy.

A
  • MRI 1st line:
    • asymmetry in size/signal on T2/FLAIR (underlying foci)
    • diffusion restriction on DWI/ADC
    • hyperintense in cortex, splenium, and/or thalamus
  • CT 2nd line [skull #, reduced GCS, focal signs, head injury, suggestion of other pathology e.g. SAH]
77
Q

Describe the differences in generalised and focal seizures [2 + 3]

A
  • generalised: rhythmic jerking, posturing, head and eye deviation, cycling movements, automatisms, vocalisation
  • focal: a seizure focus (abnormal brain structure confined to single area)
    • motor: tonic-clonic, posturing, head/eye deviation
    • sensory: somatosensory, olfactory, gustatory, visual, auditory
    • psych: memories, deja vu, jamais vu, depersonalisation, aphasia, fear
78
Q

Describe the following terms:

  • tonic
  • clonic
  • myoclonic
  • atonic
  • absence
  • simple
  • complex
A
  • tonic: stiffening
  • clonic: rhythmic movement
  • myoclonic: brief jerks
  • atonic: drop attacks, loss of postural tone
  • absence: no motor seizures
  • simple: no impaired consciousness
  • complex: impaired consciousness
79
Q

Describe the considerations of driving with epilepsy.

A
  • cannot drive a car for 6 months, or HGV/PCV for 5 years
  • 1 year from diagnosis
  • 10 years when drug-free
80
Q

Name and describe the main AEDs and their side effects.

A
  • carbamazepine: hyponatraemia, SJS in HLA-B*1502
  • lamotrigine: reduced effectiveness by COC, but safest in pregnancy
  • phenytoin: enzyme inducer
  • tolpirimate: kidney stones, teratogenic; useful in migraines
  • valproate: increased weight, tremor, teratogen; useful in migraine / mood stabiliser
81
Q

Describe status epilepticus.

A
  • > 5min of continuous seizures, or repeated seizures without return to consciousness
  • precipitants: metabolic, infection, trauma/SAH, abrupt withdrawal from AED
  • ABCDE. Serial doses with BZDs w/ glucose and thiamine
    • load phenytoin, valproate, or phenytoin
    • intubate and induce a phenobarbital coma, consider thiopentone, propofol
82
Q

Describe the clinical features and causes of UMN weakness.

A
  • CST, hemi-, quadri-, para-, monoparesis
  • central sensory loss, increased reflexes, tone, possible muscle hypertrophy
  • acute stroke, SOLs, spinal cord problems
83
Q

Describe the clinical features of causes of LMN weakness.

A
  • may be glove and stocking, peripheral nerve, root sensory loss
  • decreased reflexes, tone, increased wasting, fasciculation
  • MND, SMA, lead poisoning, polio
84
Q

Describe the differences between cerebellar gait problems and extrapyramidal problems [2].

A
  • cerebellar: broad-based, unsteady, intention tremor, dysdiadokinesis, nystagmus, dysarthria
  • extrapyramidal: TRAP, hypomimia, hypophonia, festination, impaired postural reflexes, asymmetry in PD
85
Q

Describe the key features of frontal, functional, and temporal lobe dysfunction.

A
  • frontal: personality dysfunction, paraparesis, grasp reflex, frontal gait, seizure, incontinence, visual field defect, dysphasia, anosmia
  • parietal: lower homonymous quadrantanopia, Gustmann syndrome, dyspraxia, L/R disorientation, inattention, denial
  • temporal: upper homonymous quantronopia, Wernicke’s aphasia, limbic dysfunction, temporal lobe epilepsy, auditory problems (Herschel’s gyrus)
86
Q

Name and describe the three main sleep pathologies.

A
  • REM parasomnia: lack of atonia
  • Narcolepsy: prevalence 0.04%, peaks 15 and 36. Daytime sleepiness, hypnogogic hallucination, sleep paralysis, RBD
  • cataplexy: triggered by strong emotion ad causes patients to fall to the floor.
87
Q

Name the red flags of headache histories (and their differential diagnosis).

A
  • > 55, scalp tenderness, jaw claudication, myalgia, visual symptoms [GCA]
  • cancer, immunosuppression
  • worse with cough, strain, sneezing etc.
  • thunderclap headache
  • fever, seizure, focal neurological signs, papilloedema
  • orthostatic symptoms [intracranial hypotension]
  • visual changes, pulsatile tinnitus, obesity, endocrine disease etc. [IIH]
88
Q

Describe the clinical features and diagnosis of migraine.

A
  • unilateral pulsating throbbing headache, sufficient to impede daily activities
  • lasts hours to days, may be accompanied by photo/phonophobia, N&V
  • 20-25% experience aura (most commonly visual, precedes headache, fully reversible)
  • diagnosis requires
    • 2 of moderate / severe intensity, unilateral, throbbing, worse on moving
    • 1 of autonomic features, photophobia, phonophobia
89
Q

Describe the biochemical relationship between stress and migraine.

A
  • stress triggers serotonin to be released, causing vasoconstriction
  • substance P irritates nerves and vessels and causes pain
  • the migraine centre (DRN, LC) activates the trigeminal vascular system
  • this causes vasoconstriction, release of substance P and neurokinin A
90
Q

Describe the management of migraine.

A
  • non-pharmacological: set realistic goals, keep headache diary, avoid triggers [initially worsens but will ultimately better], hydration, exercise, smoking cessation, progesterone-only contraceptive
  • abortive agents (NSAIDs, triptans, steroids; +/- antiemetic if N&V)
  • prophylaxis:
    • antidepressants (amitryptiline, SNRIs)
    • antihypertensives (propanolol, CCBs)
    • antiepileptics (topiramate, valproate)
91
Q

Describe and name the trigeminal autonomic cephalgias.

A
  • unilateral trigeminal distribution with cranial autonomic features
  • sharp stabbing facial / periorbital pain, ptosis, miosis, nasal stuffiness, N&V, eyelid oedema, conjunctival injection
    • cluster: male predominance, 1-8/day, Mx O2, triptan, steroids, prophylactic verapamil
    • paroxysmal hemicrania: 1-40/day, absolute response to indomethacin
    • hemicrania continua: female predominance, absolute response to indomethacin
    • SUNCT: short-lived, unilateral, neuralgioform, conjunctival injection, tearing; Mx lamotrigine and/or gabapentin
92
Q

Excluding the trigeminal neuralgias and migraine, name the headache syndromes.

A
  • tension type (bitemporal)
  • idiopathic intracranial hypertension
  • trigeminal neuralgia 10-100/day
  • medication overuse headache
  • occipital neuralgia: distribution over C2 nerve root, may be reproduced with percussion of the occipital condyle
  • HaNDL: headache and neuro deficits with CSF lymphocytosis; diagnosis of exclusion with spontaneous resolution
93
Q

Describe the three types of Chiari malformation.

A
  • 1: cerebellar tonsils >5mm below foramen magnum
  • 2: includes displacement of brainstem / cerebellum, causing hydrocephalus and myelomeningocele
  • 3: occipital encephalocele
94
Q

Name the risk factors for both ischaemic and haemorrhagic stroke.

A

Ischaemic
- AF, valvular disease, LVF, MI, endocarditis, Libman-Sacks, malignancy, PFO/paradoxical embolism, HTN, dissection
- vasospasm: SAH, meningitis, PRES, cocaine, marajiuana
- haematological: inherited (factor V Leiden, APLS), DIC, sickle cell, hyperviscosity, lymphoma
Haemorrhagic
- anticoagulants (warfarin higher risk than DOACs)
- chronic HTN
- coagulopathy, thrombocytopaenia, haemorrhagic conversion, cerebral venous sinus thrombosis

95
Q

Name and describe the scoring system used for ischaemic stroke.

A

Rosier score

  • LOC/syncope
  • seizure activity
  • new acute asymmetric weakness in the face [1], arm [1], leg [1]
  • speech disturbance
  • visual field defect
96
Q

Describe the investigations used for stroke.

A
  • blood glucose, chemistry, FBC, coagulation profile
  • platelets, PT / PTT (contraindication to tPA), Cr (contraindication to radiological contrast)
  • CT/MRI
  • cardiac monitor (AF)
  • agitated saline (bubble) study during echo (PFO)
  • PET/CT (malignancy)
  • LP (vasculitis)
  • blood culture (endocarditis)
97
Q

Name the blood breakdown products seen on MRI in haemorrhage stroke.

A
  • oxy-Hb
  • deoxy-Hb (1-2days); T1 med, T2 hypo
  • 1c-met-Hb (2-7days); T1 hyper, T2 hypo
  • EC-met-Hb (7-21days); T1&2 hyper
  • haemosiderin T1&2 hypo
98
Q

What are the immediate management options for ischaemic stroke.

A
  • IV tPA (<4.5hr)
  • endovascular thrombectomy, used for clots in large central vessels too large for thrombolysis (<6hr)
    • inadequate response to tPA
    • proximal occlusion (carotid, m1/proximal m2)
  • ECG/cardiac monitor, evaluate swallow, control glucose, temperature, seizure etc.
  • C/I: coagulopathy, vascular malformation, prior ICH, surgery / trauma <19d, GI haemorrhage <21d, BP >135/110
  • aspirin prevents secondary stroke
99
Q

Name and describe the scoring system used for TIA.

A

ABCD2 score:

  • age >60
  • BP >140/90
  • clinical symptoms (unilateral weakness [2], speech disturbance w/ no weakness [1])
  • DM
  • duration (>60m [2]. 10-59m [1])
100
Q

Describe the clinical management of haemorrhagic stroke.

A
  • prevent haematoma expansion by reducing BP (nicardipine)
  • reverse coagulopathy (vitamin K/warfarin, idarucizumab/dabigatran, andexanet alfa/DOACs)
  • surgical evacuation, DVT prophylaxis
101
Q

Describe the MCA distribution and symptoms of stroke here.

A
  • M1: gives off lenticulostriate, then bifurcates into M2s
  • M2 [superior]: Broca’s, motor cortex, superior visual radiation
  • M2 [inferior]: Wernicke’s, inferior visual radiation
  • most commonly affects the left side
  • R hemiplegia, hemisensory loss, aphasia, gaze deviation, R homonymous hemianopia
  • more likely to affect face/arm
102
Q

Describe the ACA distribution and the symptoms of stroke here, including MCA-ACA watershed infarct.

A
  • A1: proximal to anterior communicating
  • A2: distal
  • contralateral leg weakness, sensory loss, cognitive change
  • more likely to affect leg
  • MCA-ACA: proximal arm and leg weakness with preserved strength (‘person in a barrel’)
103
Q

Describe the PCA distribution and the symptoms of stroke here, including MCA-PCA watershed infarct.

A
  • P1 proximal to posterior communicating, P2 distal
  • contralateral homonymous hemianopia, superior quadrantanopia, impaired short term memory, alexia without agraphia
  • MCA-PCA: Ballint’s (optic ataxia, ocular apraxia, agnosia)
104
Q

Describe the features of each type of lacunar infarct.

A
  • occlusion of small penetrating arteries
  • pure motor (unilateral hemiparesis/hemiplegia)
  • pure sensory (unilateral hemisensory loss)
  • ataxia-hemiparesis (as motor)
105
Q

Name and describe the three main responses of the CNS to injury.

A
  • acute response [red neurone]: 12-24hr, results in cell death. cytoplasm is red with nuclei shrinking, chromolysis, and degeneration of the sheath
  • simple neuronal atrophy: chronic response with small dark nuclei, lipofuscin, reactive gliosis
  • gliosis: astrocyte hyperplasia and hypertrophy. nucleus enlarges and becomes vesicular
106
Q

Describe the responses of the brain to injury.

A
  • mitochondria cannot produce ATP, glutamate release raises calcium concentration, leading to proteases and oxidative stress
  • cytotoxic oedema: Na / Cl /H2O enters cells
  • ionic oedema: lack of extracellular Na/Cl causes diffusion across the BBB
  • vasogenic oedema: albumin crosses BBB
  • haemorrhagic conversion: complete failure of BBB, RBCs cross
107
Q

Describe the features of the three main types of vascular malformation.

A
  • DVA angioma: affects veins, low risk of haemorrhage
  • cavernous: affects capillaries, risk of haemorrhage, seizure, focal deficit
  • AVM: arteriovenous, no intervening capillaries; same risks as cavernous
108
Q

Describe the features of subarachnoid haemorrhage [4].

A
  • the most common cause is ruptured saccular (‘berry’) aneurysm, most commonly in arterial bifurcations
  • thunderclap headache, meningisimus, N&V, CN palsies, altered LOC, seizure
  • investigation with digital subtraction angiography
  • surgical clipping or endovascular therapy
109
Q

Describe the clinical features and management of hydrocephalus.

A
  • papilloedema, blurred vision
  • uni/bilateral CN VI palsy [false localising sign]
  • Cushing’s response (HTN, bradycardia, irregular respiration)
  • elevate head of bed to 30deg, IV hypertonic fluid, mannitol, 23% saline

6. Nervous (Neuro & Psych) (8 decks)

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