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Year 4 > Neurology > Flashcards

Neurology Flashcards

1
Q

Define stroke.

A

Sudden onset of neurological deficits of a vascular basis with infarction of CNS tissue.

  • Infarction is permanent tissue injury (confirmed by neuroimaging)
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2
Q

Define TIA

A

Sudden onset of neurological deficits of a vascular basis without infarction (i.e. resolution).

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3
Q

Describe the pathophysiology of both ischaemic and haemorrhagic strokes.

A

Ischemic

  • Arterial thrombosis: thrombus formation in artery
    • Large vessel: stenosis or occlusion of the internal carotid artery, vertebral, or intracranial arteries.
      • Mechanisms:
        • insufficient blood flow beyond lesion (haemodynamic stroke)
        • underlying processes: atherosclerosis (most common cause), dissection, and vasculitis
    • Small vessel/lacunar
      • Mechanism: Chronic HTN and DM cause vessel wall thickening and decreased luminal diameter
        • Affects mainly small penetrating arteries (primarily basal ganglia, internal capsule, and thalamus)
  • Cardioemobolic: blockage of cerebral arterial blood flow due to particles originatinbg from a cardiac source.
    • AF (most commom), rheumatic valve disease, prothetic heart vales, recent MI, fibrous and infectious endocarditis.
  • Systemic hypoperfusion (global cerebra, ischemia)
    • inadequate blood flow to brain, usually secondary to cardiac pump failure (e.g. cardiac arrest, arrythmia, or MI)
    • Primarily affects watershed aread (between the major cerebral arterial territories)

Haemorhagic

  • Intracerebral haemorrhage
    • mechanisms
      • hypertensive (most common): rupture of small microaneurysms (Charcot-Bouchard aneurysms) causing intraparenchymal haemorrhage
        • most common sites: putamen, thalamus, cerebellum, and pons
      • other: trauma, amyloid angiopathy (associated with lobar haemorrhage), vascualr malformations, vasculitis, drug us (cocaine or amphetamines)
  • Subarachnoid haemorrhage
    • ​trauma (most common)
    • spontaneous
      • ruptured aneurysms (75-80%)
      • idiopathic (14-22%)
      • AVMs (4-5%)
    • coagulopathies (iatrogenic or primary), vasculitides, tumors, cerebral artery dissections (<5%)
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4
Q

Describe stroke syndromes according to vascular territory.

ACA

A

Contralateral leg paresis and sensory loss

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5
Q

Describe stroke syndromes according to vascular territory.

MCA

A

Proximal occlusion involves:

  1. Contralteral weakness and sensory loss of face and arm
  2. Cortical sensory loss
  3. May have contralateral homonymous hemianopia or quadrantanopia
  4. If lft hemisphere: aphasia
  5. if right hemisphere: neglect
  6. eye deviation towards the side of the lesion and away from the weak side
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6
Q

Describe stroke syndromes according to vascular territory.

PCA

A
  1. Contralateral hemianopia or quadrantanopia
  2. Midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis
  3. Thalamic findings: sensory loss, amnesia, decreased level of consciousness
  4. If bilateral: cortical blindess or prosopagnosia
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7
Q

Describe stroke syndromes according to vascular territory.
Basilar artery

A

Locked-in syndrome

  1. Quadrparesis
  2. Dysarthria
  3. Impaired eye movements
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8
Q

Describe stroke syndromes according to vascular territory.

PICA (later medullary or Wallenburg syndrome)

A
  • Ipsilateral ataxia, ipsilateral Horner’s, ipsilateral facial sensory loss, contralateral limb impairment of pain and temperature sensation, nystagmus, vertigo, N/V, dysphagia, dysarthria, hiccups
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9
Q

Describe stroke syndromes according to vascular territory.

Medical medullary infarct.

A

Anterior spinal artery, which can be associated with anterior cord infarct:

  • Contralateral hemiparesis (facial sparing)
  • Contralateral imparied proprioception and vibration sensation
  • Ipsulateral tongue weakness
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10
Q

Describe stroke syndromes according to vascular territory.

Lacunar infarcts (deep hemispheric white matter)

A
  • Pure motor hemiparesis (posterior limb of internal capsule): contralateral arm, leg and face
  • Pure sensory loss (thalamic): hemisensory loss
  • Ataxic hemiparesis: ipsilateral ataxia and leg paresis
  • Dysarthria-clumsy hand syndrome: dysarthria, facial weakness, dysphagia, milh hand weakness and clumsiness.
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11
Q

Describe the general assessment of a patient with a suspected stroke?

A
  • ABCs, full vital sign monitoring, check glucose, urgent CODE STROKE if <4.5 h from symptom onset (for possible thrombolysis)
  • history
    • onset: time when last known to be awake and symptom free
    • mimics to rule out: seizure/post-ictal, hypoglycemia, migraine, conversion disorder
  • investigations
    • non-contrast CT head (STAT): to rule out hemorrhage and assess extent of infarct
    • ECG: to rule out atrial fibrillation (cardioembolic cause)
    • CBC, electrolytes, creatinine, PTT/INR, blood glucose
  • imaging (i.e. CT) signs of stroke
    • loss of cortical white-gray differentiation
    • sulcal effacement (i.e. mass effect decreases visualization of sulci)
    • hypodensity of parenchyma
    • insular ribbon sign
    • hyperdense MCA sign
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12
Q

Describe the presentations that may give clues to the aetiology of a stroke?

A
  • cerebral thrombosis is often preceded by a TIA and the neurological deficit usually progresses gradually. Headache and loss of consciousness are uncommon
  • cerebral embolism causes a sudden, complete neurological deficit.
  • Intracerebral haemorrhage causes sudden onset of headache, vomiting, stupor or coma with a rapidly progressive neurological deficit.
  • Subarachoid haemorrhage is herald by:
    • sudden, severe ‘worst headache ever’, sometimes following exertion, associated with meningism, i.e. stiff neck, photophobia, vomiting and Kernig’s sign
    • confusion or lethargy, which are common, or focal neurological deficit and coma, which are rare and serious.
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13
Q

Describe what is involved in the general assessment of a patient with suspected stroke?

A
  • ABC’s, full vital sign monitoring, check glucose, GCS, urgent CODE STROKE if <4.5 from symptom onset (for possible thrombolysis)
  • Hx
    • onset: time when last known to be awake and symptom free
    • Mimics to rule out: seizure/post-ictal, hypoglycaemia, migraine, conversion disorder.
  • Ix
    • Non-contrast CT head (STAT): to rule out haemorrhage and assess extent of infarct
    • ECG: to rule out AF (cardioembolic cuase)
    • FBC, UEC, ESR, coags, LFT, blood glucose
  • Imaging (i.e. CT) signs of stroke
    • loss of cortical white-grey differentitiation
    • sulcal effacement (i.e. mass effect decreases visualisation of sulci)
    • hypodensity of parenchyma
    • insular ribbon sign
    • hyperdense MCA sign
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14
Q

What is the management of acute stroke?

A

Within 1st hour

  • Protect airway: high dose 02 (saturate at 94%+), place NGT
  • BP: do NOT lower BP - can compromise cerebral perfusion as autoregulation is impaired. if low BP actively elevate it If on HRT, stop it.
  • Glucose: Aim for 4-11 mmol/L, sliding scale if pt is DM. Need to avoid hyperglycaemia which can increase the infarct size.
  • Temp: lower temp if febrile
  • Urgent CT/MRI
  • Thrombolysis: rtPA (recombinant tissue plasminogen activator) - alteplase 0.9mg/kg over 1 hr
    • given within 4.5 hours of acute ischaemic stroke onset provided there are clinical indications and no contraindications to use
    • Always do CT 24h post-lysis to identify bleeds
  • Anti-platelet therapy
    • Given at presentation of TIA or stroke if tPA not recieved
    • Aspirin 300mg
  • Nil by mouth till speech pathology OKs
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15
Q

What are the contraindications for tPA for a stroke?

A
  • Major infarct or haemorrhage on CT
  • Mild/non-disabling deficit
  • Recent birth, surgery, trauma or vein puncture at uncompressible site
  • Past CNS bleed
  • AVM or aneurysm
  • Severe liver disease, varices or portal hypertension
  • Seizures at presentation
  • Antigocoagulants or INR >1.7
  • Plateletes <100x109/L
  • BP >220/130
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16
Q

What is the primary prevention (before) for stroke?

A
  • Control of modifiable risk factors:
    • HTN: target BP <140/90 with ramipril 10mg PO OD
    • DM: ideal HbA1c <7%
    • Hypercholesterolaemia: statins
  • Exercise: Increased HDL and glucose tolerance.
  • Folate supplements: Help ↓ serum homocysteine
  • Quit smoking
  • Lifelong anticoagulation: if rheumatic or prosthetic heart valves on left side and chronic AF
    • risk stratifications using CHADS2 score
      • 0 (very low risk): antiplatelet
      • 1 (low risk): anticoags or antiplatelet
      • >2 (mod-high risk): anticoagulant
    • Anticoagulation therapy:
      • warfarin (titrate to INR 2-3)
      • dabigatran (110 or 150 mg bid)
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17
Q

What is involved in stroke rehabilitation?

A
  • Individualised based on severity and nature of impairment; may require inpatient program and continuation through home care or outpatient services
  • multidisciplinary approach includes dysphagia assessment and dietary modifications, communication rehabilitation, cognitive and psychological assessments including screen for depression, therapeutic exercise programs, assessment of ambulation and evaluation of need for assistive devices, splints or braces, vocational rehabilitation.
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18
Q

What is the secondary prevention for stroke? (preventing further stroke)

A
  • Antiplatelet therapy:
    • Aspirin is the inital antiplatelet of choice
    • Clopidogrel - for those who can not tolerate aspirin
  • Carotid stenosis
    • carotid endarterectomy for pt with severe stenosis (70-99%)
    • endarterectomy and carotid stenting have similar benefits but, stenting results in higher rates of stroke and endarterectomy results in higher rates of MI
  • AF: Same as primary prvention
  • HTN: Add ACEI and thiazide diuretics to ramipril and continue to aim for BP <140/90 (or <130/80 for diabetes and renal disease)
  • Hypercholesterolaemia: same as primary - use a statin, may need to increase dose if tolerated.
  • Smoking cessation: therisk of stroke decreases to baseline within 2-5 years
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19
Q

What are the differential diagnosises of headache?

Take a structured approach - consider ~10

A

Serious or life-threatening:

  • Meningitis
  • Subarachnoid haemorrhage
  • Space-occupying lesion
  • Temporal arteritis (age >50 years; ESR >50 mm/h)
  • Acute narrow-angle glaucoma
  • Hypertensive encephalopathy

Most common

  • Migraine
  • Tension or muscle contraction headache
  • Post-traumatic headache
  • Disease in other cranial structures
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20
Q

Consider your clinical approach to a pt with a headache. What infromation is important from the Hx?

A
  • Pain characertisitics: onset, frequency, duration, intensity, location, radiation, other specific features (e.g. worse in AM, worse with bending/cough/Valsalva)
  • Associated symptoms: visual changes, change in mental status, N/V, fever, meningismus, photophobia, phonophobia, TMJ popping/clicking, jaw claudication, neurological symptoms.
  • precipititating/alleviating factors (triggering factors, analgesics), medications (especially nitrates, calcium channel blockers, NSAIDs, anticoagulants), PMHx, FHx
  • red flags (possible indications for CT scan/further investigation): new-onset headache (especially if age <5 or >50), quality worse/different than previous headaches, sudden and severe (‘thunderclap’), immunocomprised, fever, focal neurological deficits, trauma
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21
Q

Consider your clinical approach to a pt with a headache. What would you look for on physical exam?

A
  • Vitals (including BP and temp), Kernig’s/Brudzinski’s, MSK examination of head and neck.
  • HEENT (head, ear, eye, nose & throat exam): fundi (papilloedema, retinal haemorrhages), red eye, temperal artery tenderness, snus palpation, TMJ
  • Full neurological exam (including LOC, orientation, pupils (symmetry), and focal neurological deficits.
  • Red flags: papilloedema, altered LOC, fever meningismus, focal neurological deficits, signs of head trauma.
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22
Q

Describe the differences between tension, migrain and cluster headaches?

A
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23
Q

What is the definition of a migraine?

A

≥5 attacks fulfilling each of the following criteria:

  • 4-72 h duration
  • 2 of the following: unilateral, pulsating, moderate-severe (interferes with daily activity), aggravated by routine physical activity
  • 1 of the following: N/V, photophobia/phonophobia/osmophobia
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24
Q

Describe the epidemiology of migraines?

A
  • 18% female
  • 6% males
  • Frequency decreases with age (especially menopause)
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25
Q

Describe the aetiology/pathophysiology of migraines?

A
  • Theories of migraine aetiology
    • Depolarisaing wave of “cortical spreading depression” across the cerebral cortex that may cause an aura (e.g. visual symptoms due to wave through occipital cortex) and also activate trigeminal nerve afferent fibres
    • Possible association with vasoconstriction/dilation
  • Significant genetic contribution
  • Triggers: stress, sleep excess/deprivation, drugs (oestrogen, nitroglycerin), hormonal changes, caffeine withdrawal, chocolate, tyramines (e.g. red wine), nitrates (e.g. processed meats)
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26
Q

Describe the signs and symptoms of a migraine?

HINT: stages and classification

A

Stages of uncomplicated migraine:

  1. prodrome (hours to days before heachache onset)
  2. aura
  3. headache
  4. postdrome

Aura:

  • fully reversible symptoms of focal cerebral dysfunction lasting <60 min
  • examples: visual disturbance (fortification spectra -zigzag; scintillating scotomata - spots), unilateral paresthesia and numbess or weakness, aphasia

Prodrome/postdrome: appetite change, autonomic symptoms, altered mood, psychomotor agitation/retardation.

Classification of migraines:

  • common migraine: no aura
  • classic migraine: with aura (heachache follows reversible aura within 60 mins)
  • complicated migraine: with severe/persistent sensorimotor deficits
    • examples:
      • basilar-type migraine (occipital headaches with diplopia, vertigo, ataxia and altered level of consciousness)
      • hmiplegic/hemisensory migraine
      • ophthalmoplegic migraine
  • acephalic migraine (i.e. migraine equivalent): aura without headache
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27
Q

What is the management of migraine?

A
  • Avoid triggers
  • mild to moderate migraine:
    • 1st line: NSAIDs (ibuprofen, naproxen)
  • moderate to severe migraine:
    • Triptans (most effective), ergots (dihydroergotamine, DHE)
  • Migraine prophylaxis: anticonvulsants (divalproex, topiramate, gabapentin), tricyclic antidepressants (amitryptiline, nortriptyline), propranolol, calcium channel blockers (verapamil)
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28
Q

Define what trigeminal autonoic cephalgia is?

A

The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomic features. The TACs include cluster headache, paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT), short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA), and hemicrania continua.

Despite their common elements, the TACs differ in attack duration and frequency, as well as the response to therapy .

  • Cluster headache has the longest attack duration (minutes to hours) and relatively low attack frequency (up to eight a day)
  • Paroxysmal hemicrania has intermediate duration (minutes) and intermediate attack frequency (up to 40 a day)
  • SUNCT/SUNA has the shortest attack duration (seconds to minutes) and the highest attack frequency (up to 200 a day)
  • Hemicrania continua (continuous daily headache for weeks to several months and sometimes years)
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29
Q

Describe the Hx and presentation of a clusert hedache?

A
  • Presents as a breif, excruciating, unilateral periobital headache that lasts 30 minutes to 3 hours, during which the patient tends to be extremly restless
  • Attacks tend to occur in clusters, affecting the same part of the head at the same time of day (commonly during sleep) and in a certain season of the year.
  • Associated symptoms include ipsilateral lacrimation of the eye, conjunctival injection, Horner’s syndrome, and nasal stuffiness
30
Q

How are cluster heachaches diagnosed?

A

Classic presentations with a history of repeated attacks over an extended period of time require no evaluation. First episodes require a workup to exclude disorders associated with Horner’s syndrome (eg, carotid artery dissection, cavernous sinus infection).

31
Q

What is the treatment and prevention of cluster headaches?

A
  • Acute therapy: High-flow 02, trypants, steroids to abort cluster.
  • Prophylactic therapy: transitional (prednisone, ergotamine), maintenance (verapmil, methysergide, lithium, valproic acid, topiramate)
32
Q

Define mutiple sclerosis.

A

A chronic inflammatory disease of the CNS characterized by relapsing remitting, or progressive neurologic symptoms due to inflammation, demyelination, and axonal degeneration

33
Q

Describe the types of course that mutiple sclerosis may take?

A
  • relapsing remitting (RRMS) 85% - most RRMS goes on to become SPMS.
  • primary progressive (PPMS) 10%
  • progressive relapsing (PRMS) 5%
  • secondary progressive (SPMS)
34
Q

Outline what is known about the pathogenesis of multiple sclerosis.

A
  • genetic
    • polygenetic: the HLA-DRB1 gene has been demonstrated to be a genetically susceptible area
    • 30% concordance for monozygotic twins, 2-4% risk in offspring of affected mother or father
  • environmental
    • MS is more common in regions with less sun exposure and lower stores of vitamin D (Europe, Canada, US, New Zealand, SE Australia)
    • MS has also been linked to certain viruses (EBV is associated with MS)
35
Q

How is multiple sclerosis diagnosed? and what are the diagnostic challengesanf factors that increase the risk of attacks?

A
  • dissemination in space and in time as based on the revised McDonald criteria
    • dissemination in time: 2 or more attacks, new gadolinium enhancing lesion 3 mo later, or new T2 lesions >1 mo after first attack
    • dissemination in space: clinical evidence of 2 or more lesions; or three of (1 gadolinium enhancing or 9 T2 lesions), (1 infratentorial lesion), (1 juxtacortical lesion), (3 periventricular lesions)
  • Investigations
    • MRI: demyelinating plaques appear as hyperintense lesions on T2 weighted MRI, with active lesions showing enhancement with gadolinium
      • typical locations: periventricular, corpus callosum, cerebellar peduncles, brainstem, juxta cortical region, and dorsolateral spinal cord
      • Dawson’s fingers: periventricular lesions extending into corpus callosum
      • cranial MRI is more sensitive than spinal MRI
    • CSF: oligoclonal bands in 90%, increased IgG concentration
    • evoked potentials (visual/auditory/somatosensory): delayed but well-preserved wave forms
  • Diagnostic challenge - patient with a single neurological episode e.g. optic neuritis, myelitis
    • important to diagnose as early treatment reduces risk of both additional attackes and disability in the longer term
    • Can show dissemination in time with a second scan with enhancing and non-enhancing lesions
  • NOTE: the risk of relapse decreases during pregnancy and increasers post-partum.
36
Q

What are the treatment options for multiple sclerosis?

A
  • acute treatment: methylprednisolone 1,000 mg IV daily x 3-7 d (no taper required); if poor response to corticosteroids may consider plasma exchange
  • disease modifying therapy
    • goals: decrease relapse rate, decrease progression of disability, slow accumulation of MRI lesions
    • first line: interferon-β (injection: Betaseron®, Avonex®, Rebif®), glatiramer acetate (injection: Copaxone®)
    • second line: natalizumab (Tysabri®) (monthly IV infusion)
    • new oral agents: fingolimod (available) and cladribine (not yet available)
      • indications for fingolimod: newly diagnosed patients with active RRMS who prefer oral treatment despite increased risks or those intolerant of first line therapies
    • CIS: early treatment with interferons may delay potential second attack
    • RRMS: DMT reduces rate of relapse by about 30%
    • PPMS/SPMS: no proven efficacy of DMTs
  • symptomatic treatment
    • spasticity: baclofen, tizanidine, dantrolene, benzodiazepine, botulinum toxin
    • bladder dysfunction: oxybutynin
    • pain: TCA, carbamazepine, gabapentin
    • fatigue: amantidine, modafinil, methylphenidate
    • depression: antidepressant, lithium
    • constipation: high fiber intake, stool softener, laxatives
    • sexual dysfunction: sildenafil, tadenafil, vardenafil
  • education and counseling: MS Society, support groups, psychosocial issues
37
Q

Describe the prognosis of multiple sclerosis?

A
  • good prognostic indicators: female, young, RRMS, presenting with optic neuritis, low burden of disease on initial MRI, low rate of relapse early in disease
  • PPMS: poor prognosis, higher rates of disability, poor response to therapy
38
Q

Define what Guillain-Barre syndrome is?

A
  • An acute, rapidly progressive, acquired demyelinating autoimmune disoder of the peripheral nerves that results in weakness.
  • Also known as acute inflammatory demyelinating polyneuropathy.
  • Associated with recent Campylobacter jejuni infection, viral infection, or influenza vaccination.
  • Approximately 85% of patients make a complete or near-complete recovery (may take up to 1 year). The mortality rate is < 5%.
39
Q

Describe the signs and symptoms of Guillain-Barre Syndrome?

A
  • Classically presents with progressive (over days), symmetric, ascending paralysis (distal to proximal) involving the trunk, diaphragm, and cranial nerves. Atypical presentations are common, including variants that begin with cranial involvement or progress unpredictably to involve the respiratory muscles.
    • Sensory: distal and symmetric paresthesias, loss of proprioception and vibration sense,
      neuropathic pain
    • motor: weakness starting distally in legs, areflexia
  • Autonomic dysregulation, areflexia, and dysesthesias may be present.
    • autonomic: blood pressure dysregulation, arrhythmias, bladder dysfunction
40
Q

What are the 5 A’s of Guillain-Barre syndrome?

A
  • Acute inflammatory demyelinating polyradiculopathy
  • Ascending paralysis
  • Autonomic neuropathy
  • Arrhythmias
  • Albuminocytologic dissociation
41
Q

How is Guillain-Barre syndrome diagnosed?

A
  • CSF: albuminocytological dissociation (high protein, normal WBC)
  • EMG/NCS: conduction block, differential or focal (motor > sensory) slowing, decreased F-wave, sural sparing
  • Brain and spinal cord MRI
42
Q

What are the DDx for a patient presenting withsymmetric polyneuropathy?

A
  • vascualr
    • Polyarteritis nodosa
    • SLE
    • Rheumatoid artheritis
  • Infectious
    • HIV
    • Leprosy
  • Immune
    • Guillain-barre syndrome
    • Chronic inflammatory demyelinating polyneuropathy
  • Hereditary: Hereditary motor and sensory neuropathy
  • Neoplastic:
    • Paraneoplastic
    • Myeloma
    • Lymphoma
    • Monoclonal gammopathy
  • Toxin
    • EtOH
    • Heavy metals - lead
    • Medications: amiodarone, metronidazole
  • Metabolic:
    • DM
    • Hypothyroidism
    • Renal failure
  • Nutritional
    • B12
    • Vit E
    • Thiamine
  • Other:
    • Porphyria
    • Amyloid
43
Q

Describe the pathophysiology of Guillane-Barre syndrome?

A
  • Autoimmune attack and damage to peripheral nerve myelin
  • Sometimes preceded by viral/bacterial infections - most common antecedent infection is Campylobacter jejuni
44
Q

What is the treatment of a patient with Guillan-Barre syndrome?

A
  • Admit to ICU for cases of impending respiratory failure
  • Plasmapheresis and IVIG are first-line treatments. Corticosteroids are NOT indicated
  • Aggressive physical rehab is imperative
45
Q

Describe the treatment for neuropathic pain?

A
  • Identify/treat underlying cause
  • Pharmacotherapy
    • Anticonvulsant: pregabalin, gabapentin, sodium valproate
    • Antidepressants: amitriptyline, venlafaxine, duloxetine
    • Opiods: dextromethorphan, morphine sulphate, tramadol, oxycodone
    • Other: capsaicin and isosorbide dinitrate spray
  • Non -pharmacologic therapies
    • percutaneous electrical stimulation (moderate evidence)
    • neuropsychiatry: CBT, psychotherapy
    • Rehabilitation: physiotherapy
  • Surgical therapies:
    • Dorsal column neurostimulator
46
Q

What is the difference between chronic inflammatory demyelinating polyradiculopathy (CIDP) and Guillain-Barre syndrome?

A
  • When GBS is severe enough to cause degeneration of the whole nerve fibre. In these patients the recovery is often slower and incomplete. A chronic form GBS may present with progressive symptoms and result in CIDP
  • GBS develops rapidly, CIDP is slowly progressive with diffuse sensory and motor symptoms
  • Diagnosis:
    • CIDP will need nerve biopsy, GBS does not
  • CIDP respondes to corticosteroids unlike GBS
47
Q

Define dementia (major neurocognitive disorder).

A
  • An acquired, generalised and (usually) progressive impairment of cognitiv function (i.e. memory, recall, orientation, language, abstraction) associated with impairment in activities of daily living (i.e. planning, shopping, food preparation, difficulties with finances)
  • Affects comprehension, but not level of consciousness.
  • Diagnosis of dementia requires presence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:
    • Concern of the individual or a knowledgeable informant AND
    • A substantial impairment in cognitive performance either documented by standardised neuropsychological testing or quantified clinical assessment.
48
Q

State community prevalence of dementia by age group and predict how many people will have dementia in Australia by 2030.

A
  • Prevalence is 1-2% at age 65 and reaching 30% by age 85.
  • By 2030, an estimated 465,000 people will have dementia in Australia
49
Q

Compare and contrast clinical features of dementia and delirium.

A
50
Q

Detail the classification of dementia.

A
  • Primary degenerative:
    • Alzheimer’s disease
    • Dementia with Lewy bodies
    • Frototemporal dementia (e.g. Pick’s disease)
    • Huntington’s disease
  • Vascular
    • Vascular cognitive impairment (previously multi-infarct dementia)
    • CNS vasculitis
  • Infection:
    • Chronic meningitis
    • Chronic encephalitis
    • Chronic abscess
    • HIV
    • Creutzfelt-Jacob disease
    • Syphillis
  • Traumatic - diffuse axonal shear, epidural haematoma, subdural haematoma
  • Rheumatologic: SLE
  • Neoplastic
    • Mass effect/oedema, haemorrhage, seizure
    • Paraneoplastic encephalitis
51
Q

Outline the methods used to diagnose dementia.

A
  • Hx
    • “Geriatric giants”
      • Confusion/incontience/falls/polypharmacy
      • Memory and safety (wandering, leaving doors unlocked, leaving stove on, losing objects)
      • Behavioural (mood, anxiety, psychosis, suicidal ideation, personality changes, aggression)
    • ADLs and IADLs
    • Cardiovascular, endocrine, neoplastic, renal review of systems.
    • Alcohol and smoking
    • OTCs, herbal remedies, medications (sedative, hypnotics, antipsychotics, antidepressants, anticholinergics), compliance, accessibility
    • Hx of vascualr disease or head trauma
    • collateral Hx
  • Physical exam
    • BP
    • Hearing and vision
    • Neurological exam with attention to signs of parkinsonism, UMN findings, cerebravascular disease
    • General phsyical exam depending on risk factors and Hx
    • MMSE or MoCA, clock drawing, frontal lobe testing (go/no go, words lists, similarities, proverb)
  • Investigations
    • Blood test: FBC, glucose, TSH, B12, Folate, UEC, LFT, lipids, serum calcium
      • If clinically indicated: VDRL (syphillis), HIV, ANA, anti-dsDNA, ANCA, ceruloplasmin, copper, cortisol, toxicology, heavy metals
    • ECG
    • Imaging: CXR, CT head and/or MRI
  • issues to consider
    • failure to cope, fitness to drive, caregivers education and stress, power of attorney
52
Q

Describe the clinical features of dementia depending on localisation.

A
53
Q

Describe the progression of Alzheimer’s disease?

A
  • Most common presentation – amnesia, in particular a failure of anterograde episodic memory
  • Early AD – delayed recall (e.g. name and address after 5 minutes), good working memory, depression - As disease progresses – progressive disturbance of semantic memory, impaired verbal fluency, impaired remote memory (famous faces and events)
  • Middle stages of the disease – visual and perceptual difficulties, ideomotor apraxia (dressing and eating difficult), language skills decline, paucity of speech evidence, comprehension impaired, and reading, writing and calculation all become affected
  • Advanced disease – akinesia, rigidity, myoclonus (involvement of cortical and subcortical structures)
54
Q

What psychiatric symptoms are present in pts with Alzheimer’s disease?

A
  • Behavioural and psychiatric manifestations (80% of those with major dementia)
    • mild dementia: major depressive disorder and/or apathy
    • major dementia: psychosis, irritability, agitation, combativeness, and wandering.
55
Q

Describe Lewy body dementia and its treatment?

A
  • A neurocognitive disease that includes not only progressive cognitive impairment (with early changes in complex attention and executive function rather than learning and memory), but also recurrent complex visual hallucinations
  • Core diagnostic features
    • Fluctuating cognition with pronounced variations in attention and alertness
    • Recurrent visual hallucinations that are well formed and detailed
    • Spontaneous features of parkinsonism, with onset subsequent to development of cognitive decline
  • Treatment – acetylcholinesterase inhibitors (e.g. donepezil)
56
Q

Describe frontotemporal dementia.

A
  • Refers to a group of disorders caused by progressive cell degeneration in the frontal or temporal lobes
  • Behavioural variant – most common, disinhibition and apathy common
  • Language variant – prominent decline in language ability, in the form of speech production, word finding, object naming, grammar, or word comprehension
  • Movement disorders
    • Corticobasal degeneration (CBD) – shakiness, lack of coordination, muscle rigidity and spasms
    • Progressive supranuclear palsy (PSP) – walking and balance problems, frequent falls and muscle stiffness
57
Q

Describe vascular dementia.

A
  • Diagnosis of major or mild NCD with determination of cerebrovascular disease as the dominant if not exclusive pathology that accounts for the cognitive defects
  • Second most common cause of NCD
  • Vascular aetiology suggested by one of the following:
    • Onset of cognitive deficits is temporally related to one or more cerebrovascular events
    • Evidence for decline is prominent in complex attention (including processing speed) and frontalexecutive function
  • For mild vascular NCD – history of a single stroke or extensive white matter disease is sufficient
  • For major vascular NCD – history of two or more strokes, a strategically placed stroke, or a combination of white matter disease, and one or more lacune is generally necessary
58
Q

Describe the DDx of seizure?

A
  • Syncope (especially convulsive)
  • TIA/stroke
  • Migraine
  • Transient global amnesia
  • Panic attack
  • Pseudoseizure
  • Behavioural automatisms/tics
  • Sleep, sleep-walking
  • Metabolic disturbance (hypoglycaemia)
  • Retrograde amnesia (in association with an accident
59
Q

Compare and contrast syncope and seizures.

A
60
Q

Define epilepsy and outline the features of provoked/unprovoked seizures.

A
  • Seizure – paroxysmal cerebral event resulting from abnormal, involuntary, rhythmic neuronal discharges, (usually) causing altered behaviour, sensations or awareness
  • Provoked seizure – a seizure occurring in a previously normal brain because of an abnormal physiological stress (metabolic insult, drugs, acute neurological illness)
  • Unprovoked seizure – a seizure occurring in the absence of an identifiable acute insult
  • Epilepsy – a disorder predisposing to recurrent (≥2) unprovoked seizures.
61
Q

Summarise the lifetime risk of having a seizure.

A
  • ~10% of population have at least one seizure
  • 1-3% of population develop epilepsy at some stage in their lives
  • The risk of a second seizure after a first unprovoked seizure is ~30-50%
  • The risk of a third seizure after a second unprovoked seizure is ~70-75%
  • The incidence and prevalence of epilepsy depend on age and the specific subtype of epilepsy
62
Q

Differentiate between LMN, UMN and extrapyramidal lesions.

A
63
Q

For the deep tendon reflexes: what muscle tendon corrilates to which nerve root?

A
64
Q

What bloods need to be ordered to investigated the underlying cause of a stroke?

A
  • FBC: exclude polycythaemia and essential thrombocythaemia
  • Cholesterol and triglycerides
  • BSL
  • Homocysteine
  • Cardiolopin Ab
  • Lupus anticoagulant: exclude antiphospholipid syndrome
  • PHN screen by flow cytometry
  • HLA B27: Behcet’s disease
65
Q

What imaging is used to investigate stroke?

A
  • CT
  • Carotid doppler
  • MRI, MRA, MRV
  • cardiac investigation: ECG, holter monitor, echocardiography
66
Q

What are the extrapyramidal signs?

A
  • Tremour
  • Bradykinesia (slowness of movements)/ Akinesia
  • Rigidity
  • Akathisia (motor restlessness)
  • Festinant gait
  • Distonia (continuous spasms and muscle contractions)
  • Tradive dyskinesia (irregular, jerky movements)
67
Q

Lesions in the frontal lobe cause what issues?

A

Difficulties with task sequencing and executive skills:

  • Expressive aphasia (receptive aphasia is due to a temporal lobe lesion)
  • Primitive reflexes
  • Perseveration (repeatedly asking the same question or performing the same task)
  • Anosmia
  • Changes in personality.
68
Q

Lesions in the parietal lobe cause what issues?

A
  • Apraxias
  • Neglect
  • Astereognosis (unable to recognise an object by feeling it)
  • Visual field defects (typically homonymous inferior quadrantanopia).
  • may also cause acalculia (inability to perform mental arithmetic).
69
Q

Lesions in the temporal lobe cause what issues?

A
  • Visual field defects (typically homonymous superior quadrantanopia)
  • Wernicke’s (receptive) aphasia
  • Auditory agnosia
  • Memory impairment.
70
Q

LEsions in the occipital lobe cause what issues?

A
  • Cortical blindness (blindness due to damage to the visual cortex and may present as Anton’s syndrome where there is blindness but the patient is unaware or denies blindness)
  • Homonymous hemianopia
  • Visual agnosia (seeing but not perceiving objects - it is different from neglect, since in agnosia the objects are seen and followed but cannot be named).
71
Q
A
72
Q
A

Year 4 (25 decks)

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