Neurology - Disorders Flashcards

1
Q

Discuss possible etiology for new onset seizure

A
  • stroke
  • intra-cranial hemorrhage
  • head trauma
  • alcohol withdrawal
  • brain tumour
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2
Q

Discuss the definition of status epilepticus

A

Any of the following
- single epileptic seizure lasting >30 minutes in duration
- series of epileptic seizures during which function is not regained between ictal events in 30 minute period
Clinically any of the following
- >5 minutes of continuous seizure
- >=2 discrete seizures between which there is incomplete recovery of consciousness

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3
Q

Discuss the ABC and initial investigations for seizure

A
Stabilization
- intubation if vomiting or failure to ventilate/oxygenate
- supplemental oxygen
- initially have hypertension which switch to hypotension post-ictal which may need ephedrine/phenylephrine
Investigations
- CBC, electrolytes
- blood glucose
- blood toxicology screen
- LFT, creatinine BUN
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4
Q

Discuss the management of seziure

A

Initial Therapy
- Lorazepam 0.1mg/kg
- Diazepam 0.1mg/kg
- Midazolam 0.05mg/kg (10kg IM if no IV access and >40kg)
- Fosphenytoin 20mg/kg in second IV
- No benefit with benzodiazepine then try second benzodiazepine after 1 minute
Refractory
- require intubation, mechanical ventilation, continuous EEG monitoring
- Midazolam (does not lower BP) 0.2mg/kg IV
- Can infuse at 0.1mg/kg/hr and titrate upward until seizure done
- Propofol 1-2mg/kg loading dose over 5 minutes then titrate to 10-12mg/kg/hr until seizure stops
- Pentobarbital 5mg/kg over 10 minutes and repeat until stops

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5
Q

Discuss the presentation and management of seizure

A

Presentation
- trigger, prodrome, ictal movements, post-ictal period
Investigation
- ECG for all with loss of consciousness
- EEG for all that do not return to normal level of consciousness
- CT if focal deficit
- headache then lumbar puncture
Management
- should not drive home
- start long-acting anti-convulsant if discharged home

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6
Q

Discuss the presentation and management of meningitis

A
Etiology
- strep pneumonia
- neisseria meningitidis
- hemophilus influenza
Presentation
- triad of headache, fever, stiff neck
- photophobia
- seizure
- petechial rash in meningitis
- cranial nerve abnormality if involve brainstem
- nuchal rigidity
- positive Kernig (thigh and knee at 90 and pain with resisted knee extension)
- positive Brudzinski (flexion of neck elicits flexion at hips)
Investigation
- Lumbar puncture demonstrating
    - High WBC with neutrophils
    - low glucose, high protein, high lactate
    - Gram stain and culture
Management
- <50 IV ceftriaxone with vancomycin
- >50 and immunocompromised IV ceftriaxone, vancomycin, ampicillin
- Dexamethasone 
- Intracranial pressure control
     - Elevate head of bed
     - control BP
     - Glycerol/Mannitol if ICP >20
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7
Q

Discuss the differential for Delirium

A

I WATCH DEATH

  • infection (UTI, pneumonia)
  • Withdrawal (alcohol, benzodiazepines)
  • Acute metabolic disorder (electrolyte imbalance, kidney or renal failure)
  • Trauma
  • CNS pathology (stroke, hemorrhage, tumour)
  • Hypoxia
  • Defieciences (thiamine, vitamin B12)
  • Endocrinopathies (thyroid, glucose, adrenal)
  • Acute vascular
  • Toxins, substance use
  • Heavy metals
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8
Q

Discuss the diagnostic criteria for delirium

A

Disturbance in attention or awareness
- change in baseline
- reduced ability to focus, sustain and shift attention
- in awareness with reduced orientation to environment
Disturbance is acute and fluctuates
Cognitive decline in any domain
No other condition or substance

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9
Q

Discuss the management of delirium

A
History
- baseline function
- time course of cognitive change
- medical conditions
- medications (gravol, benzodiazepines, and susbtances)
- collateral
Investigations
- CBC
- electrolytes
- calcium
- magnesium
- phosphate
- TSH
- folate
- vitamin B12
- glucose
- creatinien, urea
- liver enzymes
- urinalysis and culture
- ECG
- CXR
Reverse Cause
- correct sensory deficits
- monitor constipation and urinary retention
- fluids and nutrition
Control Symptoms
- behavioural management
- family to visit
- mobilize
- prefered language with clear and simple communication
- haldol 0.5-1mg with max of 3-4mg/24hrs until sedation achieved and then maintenance for 24 hours
- atypical antipsychotics (must do ECG where QTc >450 or >25% increase from baseline then discontinue)
- Benzodiazepines used in elderly to prevent QTc prolongation
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10
Q

Discuss the diagnostic algorithm for vertigo

A
Ask about migraines
- if present then migranous vertigo
Ask about hearing loss
- present then ask about episodic
       - present then meniere disease
       - absent then labyrinthitis
- no hearing loss ask about episodic
       - present the benign paroxysmal positional vertigo
       - absent then vestibular neuritis
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11
Q

Discuss diagnostic algorithm for dysequilibrium

A
Underlying condition
- peripheral neuropathy
- Parkinson's
- medications
Older Individuals Evaluate
- gait
- vision
- Romberg test
- neuropathy screen
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12
Q

Discuss the diagnostic algorithm for presyncope

A

Cardiovascular history

  • arrhythmia
  • myocardial infarction
  • medication
  • orthostatic hypotension
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13
Q

Discuss the diagnostic algorithm for lightheadedness

A
  • history of depression or anxiety

- hyperventilation provocation test

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14
Q

Differentiate between upper and lower motor neuron disease

A
Upper Motor Neuron
- Minimal muscle atrophy
- increased tone, spasticity
- hyperreflexia
- upgoing plantar response
Lower Motor Neuron Disease
- weakness, muscle atrophy
- decreased tone
- hyporeflexia
- downgoing plantar reflex (normal)
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15
Q

Differentiate between motor, sensory and autonomic neuropathy

A
Motor
- muscle weakness
- atrophy
- cramps
Sensory
- numbness
- loss of feeling
- tingling paresthesia
- small fibers have more burning pain, large then loss of proprioception
Autonomic
- sweating
- gastroparesis
- bowel/bladder dysfunction
- erectile dysfunction
- orthostatic hypotension
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16
Q

Discuss causes of mononeuropathy

A
Compressive Neuropathy
- carpal tunnel syndrome
- ulnar neuropathy
- radial nerve (saturday night palsy)
- lateral femoral cutaneous nerve
- peroneal neuropathy
Mononeuropathy Multiplex
- diabetes mellitus
- rheumatoid arthritis
- SLE
- vasculitis
17
Q

Discuss causes of polyneuropathy

A
Axonal Polyneuropathy
- diabetes
- renal failure
- vitamin B12 deficiency
- alcohol
Demyelinating Polyneuropathy
- Guillain-Barre syndrome
              - acute progressive symmetric muscle weakness with hyporeflexia
- Chronic Inflammatory Demyelinating polyneuropathy
18
Q

Differentiate between different types of focal seizures

A

Focal with Intact Awareness
- Jacksonian march where spreading to adjacent muscle groups
- Unusual sensations
Focal with Impaired Awareness
- may appear awake but impairement of awareness
- automastims: chewing, swallowing, lip-smacking

19
Q

Discuss the pathophysiology, presentation and management of Parkinson’s

A

Pathophysiology
- loss of dopaminergic neurons in pars compacta of substantia nigra leads to decreased dopamine in striatum and disinhibition of indirect pathway and decreased activation of the direct pathway
- Results in increased inhibition of cortical motor areas
Presentation (TRAP)
- Tremor, resting pill-rolling
- Rigidity: lead-pipe, cogwheeling
- Akinesia/bradykinesia: slow, small amplitude movements, fatigue of rapid alternating movements
- Postural instability: shuffling gait, freezing of gait
Management
- Levodopa/carbidopa where levodopa is dopamine precursor and carbidopa decreases peripheral metabolism of levodopa decreasing side effects and increasing half-life

20
Q

Discuss the pathophysiology, presentation and management of Huntingtons Disease

A

Pathophysiology
- autosomal dominant CAG repeats on Huntington gene on chromosome 4
- have global cerebral atrophy, worse in striatum leading to increased activity of direct pathway and decreased indirect pathway
Presentation
- clumsiness, fidgetiness, irribility to major NCD, psychosis and chorea
- Chorea: begins with movement of eyebrows and forehead to dance-like or ballism to rigidity and dystonia
Investigation
- MRI: enlarged ventricles, atrophy
Management
- no disease altering treatment

21
Q

Discuss the pathophysiology, presentation and management of dystonia

A

Presentation
- sustained twitching movements caused by co-contraction of agonist and antagonist
- worsened with fatigue, stress, and emotions
Management
- Botox
- anticholinergics, muscle relexants

22
Q

Discuss the pathophysiology, presentation and management of amyotrophic lateral sclerosis

A
  • progressive neurodegenerative disease of UMN and LMN
    Pathophysiology
  • anterior horn cells, cranial nerve nuclei and corticospinal tract affected
    Presentation
  • Limb motor movements: segmental and asymmetrical UMN and LMN
  • Bulbar: dysarthria, dysphagia, tongue atrophy and fasciculations
  • Frontotemporal dementia
  • Sparing of sensation, ocular muscles, bowel/bladder sphincters
    Investigations
  • EMG: chronic denervation and reinnervation, fasciculations
    Management
  • riluzole
  • BiPAP
  • spasticity: baclofen, tizanidine
23
Q

Discuss the pathophysiology, presentation and management of Guillain-Barre Syndrome

A

Pathophysiology
- acute rapidly evolving inflammatory polyradiculopathy that starts distal lower limbs and ascends
- autoimmune attack of myelin following viral/bacterial infection
Presentation
- Distal symmetric paresthesias, loss of proprioception
- weakness and areflexia
- autonomic: blood pressure dysfunction
Investigations
- CSF: albuminocytologic dissociation (high protein, normal WBC)
Management
- IVIG or plasmaphoresis

24
Q

Discuss the pathophysiology, presentation and management of myasthenia gravis

A

Pathophysiology
- progressive autoimmune disorder due to anti-ACh or anti-MuSK anitbodies resulting in early saturation of the neuromuscular junction and inadequate muscle activation with increasing nerve stimulation
- increase risk of thymic neoplasia
Presentation
- Fatigable, weakness without reflex changes, sensory changes or coordination abnormalities
- diplopia or ptosis
- dysphagia or dysarthria (bulbar muscles)
- proximal limb weakness
Investigations
- Edrophonium test: improvement over 2min following injection
- ECG: decremental response with increased stimulation
- Anti-ACh antibody assay
- CT/MRI for thymic dysplasia
Management
- acetylcholinesterase inhibitors (pyridostigmine)
- steroids

25
Q

Discuss the pathophysiology, presentation and management of Lambert-Eaton Myasthenic Syndrome

A

Pathophysiology
- autoimmune disorder due to antibodies against presynaptic voltage-gated calcium channels, causing decreased ACh at the NMJ
- associated with small-cell carcinoma of the lung
Presentation
- Weakness of skeletal muscle without sensory or coordination abnormalities
- reflexes diminished or absent
- dry mouth, impotence, constipation, blurred vision
Investigations
- no response with edrophonium test
- EMG: incremental response with rapid stimulation
Management
- ACh modulation

26
Q

Discuss the pathophysiology, presentation and management of botulism

A
Pathophysiology
- clostridium botulinum bacteria enter through wounds or ingestion
PResentation
- 6-48hr following ingestion
- GI symptoms to EOM weakness to dysphagia to limbs and respiratory involvement
- dry mouth
Investigation
- blood test for toxin
Treatment
- botulinum anti-toxin
27
Q

Discuss the pathophysiology, presentation and management of myotonic dystrophy

A

Pathophysiology
- unstable trinucleotide CTG repeat in myotonic dystrophy kinase gene
Presentation
- ptosis, bifacial weakness, frontal baldness and triangular faces
- distal muscle weakness worse
- delayed relaxation of muscles after exertion
- heart block and atrial arrthymias
- hypoventilation

28
Q

Discuss the pathophysiology, presentation and management of complex regional pain syndrome

A

Pathophysiology
- minor injury to limb or lesions in remote body area precede symptoms
Presentation
- continuing pain with allodynia and hyperalgesia
- edema, changes in skin blood flow, or abnormal vasomotor activity
Management
- early mobilization
- topical capsaicin
- TCA

29
Q

Discuss the clinical patterns and diagnosis of multiple sclerosis

A
  • chronic inflammatory disease of CNS characterized by relapsing and remitting neurological symptoms due to inflammation, demyelination and axonal degeneration
    Clinical Pattern
  • relapsing remitting
  • primary progressive
  • progressive relapsing
  • secondary progressive
    Diagnosis
  • Dissemination in time: 2 or more attacks with presence of gadolinium enhancing and non-enhancing MRI lesions at any time
  • Dissemination in space: >=1 T2 lesions in MRI in at least 2 of 4 CNS regions (periventricular, juxtacortical, infratentorial, spinal cord)
30
Q

Discuss the presentation and management of multiple sclerosis

A

Presentation
- numbness, optic neuritis, weakness, spasticity, weakness
- Lhermitte’s sign
- Uhthoff’s phenomenom
Investigation
- MRI: demyelinating plaques appear hyperintense on TW
- dawson’s fingers with periventricular lesions heading into corpus callosum
- CSF: oligoclonal bands
- evoked potentials delayed
Management
- Acute: methyprednisolone 1000mg IV x3-7d
- Disease modifying: teriflunomide, interferon B
- Symptomatic: baclofen, oxybutynin for bladder dysfunction, TCA