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Phase 4 > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the clinical features of parkinsonism?

A 
Resting tremor:
-coarse
-pill rolling
-asymmetrical
Bradykinesia:
-slowed movement
Postural instability
Rigidity:
-cogwheel or leadpipe
Hypomima
Festinant gait:
-shuffling, reduced arm movement
Speech quiet and monotonous
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2
Q

What is the main cause of a resting tremor?

A

Parkinsonism

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3
Q

What are the causes of postural tremor (worse with arms outstretched):

A 
Benign essential tremor (worse with arms stretched out)
Anxiety
Thyrotoxicosis
Metabolic: CO2 retention
Alcohol
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4
Q

What is the main cause of intention tremor?

A

Cerebellar disease.

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5
Q

What are the causes of parkinsonism?

A

Idiopathic parkinson’s disease.
Drug induced: dopaminergic receptor blockers, anti-psychotics/anti-emetics
Parkinson’s plus: multisystem atrophy, progressive supranuclear palsy, corticobasal degeneration.
Post encephalitic parkinsonism
Vascular parkinsonism

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6
Q

What is the pathology of idiopathic parkinson’s?

A

Degeneration of dopaminergic neurones between the substantia nigra and basal ganglia.
Deficient in dopamine (excitatory neurotransmitter) in the basal ganglia
Overall increased inhibitory output and decreased cortical activity.

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7
Q

What are the other symptoms of parkinsons disease?

A 
Depression
Fatigue
Hyposmia/anosmia
Autonomic dysfunction:
constipation
incontinence
dysphagia
sleep disturbance
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8
Q

How is parkinsons diagnosed?

A 
Clinical diagnosis:
Bradykinesia plus one of rigidity, rest tremor and postural instability. 
Absence of atypical features
Slowly progressive course
Response to drug therapy.
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9
Q

What are the investigations of parkinsons?

A 
DAT-SPECT scanning
CT or MRI
 - structural cause of symptoms
 - degree of cerebrovascular disease
 - MRI can help identify some parkinson's plus
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10
Q

What are the treatments of parkinsons?

A 
L-dopa
Pramiprexole
Ropinirole
MAO-B inhibitor e.g. selegiline
COMT inhibitors e.g. entacapone
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11
Q

How does L-dopa work?

A

Converted to dopamine in brain.
Used with decarboxylase inhibitor e.g. carbidopa, to prevent peripheral breakdown and reduce side effects like nausesa.
Effects wear out over years
Problems with on/off motor fluctuations - some modified release formulas help.

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12
Q

How do pramiprexole and ropinirole work?

A

Activate dopamine receptors.
Fewer side effects than L-dopa
Use in younger patients to save L-dopa for later.
Apomorphine can be given by SC injection or pump
Rotigotine as paatch can be used if patients unable to swallow

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13
Q

How do MAO-B inhibitors work?

A

Inhibit the enzyme MAO-B which breaks down dopamine.

Can be used to delay need for L-dopa and also works well with L-dopa

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14
Q

How do COMT inhibitors work?

A

Catechol-O-methyltransferase inhibitors prevent peripheral breakdown of L-dopa, reduces motor fluctuations.
Smooth out the action of L-dopa

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15
Q

What are the more invasive treatments of Parkinson’s?

A

Apomorphine subcut infusion (dopamine agonist)
Intraduodenal levodopa
Neurosurgery e.g. deep brain stimulation.

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16
Q

What is the prognosis of parkinsons?

A

Progressive neurodegenerative disease.
Typical course:
2-3 years with resolution of symptoms with dopaminergic agents.
Motor compliments after 5 years of levodopa treatment.
After a number of years - freezing, falling and dementia, not responsive to levodopa
Cognitive dysfunction

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17
Q

What are the predictors of parkinsons progression?

A

Tremor predominance, slower progression.
Rapid rate of progression:
- older age at symptom onset
- rigidity/hypokinesia as presenting symptoms
- associated comorbidities
- decreased response to dopaminergic medications

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18
Q

What is Lewy body dementia?

A

Progressive cognitive decline to interfere with normal living, hallucinations, fluctuating mental status.

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19
Q

What are the typical core features of Lewy Body dementia?

A

Fluctuating cognition
Recurrent visual hallucinations
REM sleep behaviour disorder
and one or more spontaneous symptoms of parkinsonism: bradykinesia, rest tremor, or rigidity.

20
Q

What are the features of progressive supranuclear palsies?

A

Gaze palsies and early falls within 1 year of diagnosis.

Vertical gaze palsy and significant postural instability.

21
Q

What are the features of vascular parkinsonism?

A

Lower extremity prominence of symptoms.
Symmetric symptoms.
Stepwise progression.
Less responsive to levodopa.

22
Q

What is delirium?

A

Acute confusional state. Impairment of attention and consciousness accompanied by abnormalities of perception and mood. Fluctuating course.

23
Q

What is dementia?

A

Generalised and progressive impairment of memory, intellect, and personality and has not loss of consciousness.

24
Q

Which neurotransmitters can be affected in delirium?

A

Cholingeric
Dopaminergic
Adrenergic
GABAergic

25
Q

What is the pathogenesis of delirium?

A

Primed microglial cells have exaggerated response to pro-inflammatory mediators.
Evidence of increased dopaminergic signalling with psychotic features.
Inflammatory cytokines impair neurotransmission (elevated levels of IL-6 and IL-8 are found in patients who develop delirium including post hip fracture).
High cortisol has been shown to be associated with mental status deterioration.

26
Q

What are the subtypes of delirium?

A

Hyperactive

Hypoactive

27
Q

What are the predisposing factors for delirium?

A 
Extremes of age
Vulnerable brain (e.g. dementia, head injury, alcohol excess, stroke)
Change in environment
Sleep deprivation
Immobilisation/hip fracture
Serious illness
Sensory deprivation
Polypharmacy
Frailty
28
Q

Which factors can prolong delirium?

A 
Immobility
Use of physical restraint
Use of bladder catheter
Iatrogenic events
Malnutrition
Psychoactive medications
Intercurrent illness
Dehydration
29
Q

What are the differential diagnosis of delirium?

A 
Dementia
Depression
Mania
Schizophrenia
Dysphasia
Non convulsive epilepsy/temporal lobe epilepsy
Hepatic encephalopathy
30
Q

What is the environmental management of delirium?

A 
Well lit, single room
Familiar staff, re-orientation
Hearing aids, glasses etc. 
Family
Music
Mobilisation - 20 mins BD at least
Preservation of sleep wake cycle
31
Q

What is the pharmacological management of delirium?

A

Replace electrolytes.
Antibiotics if indicated
Pabrinex, diazepam, chlordiazepoxide etc if alcohol induced.
Anti-epileptics if seizures.
Laxatives if necessary
Stop offending drugs if possible.
If danger to self can use haloperidol, avoid benzodiazepines.
Do not use anti-dopaminergics in Parkinson’s patients and Lewy body.

32
Q

Which investigations would be done for a subarachnoid haemorrhage?

A

CT scan
Lumbar puncture (xanthochromia after 12 hours)
CT angiography
MR angiography

33
Q

What is the management of subarachnoid haemorrhage?

A

Headache should be treated with opiods.
Calcium channel blockers should be stared on admission for vasospasm prophylaxis.
Most surgeons operate on patients with good neurological status within the first 72 hours to prevent re-bleeding: surgical clipping or coil embolisation

34
Q

What are the complications of subarachnoid haemorrhage?

A 
Re bleeding
Acute hydrocephalus
Vasospasm
Venricular wall motion abnormalities
Pulmonary oedema
Seizures
Cognitive impairment
35
Q

What is the mortality of subarachnoid haemorrhage?

A

1 in 4 dead at 6 months.

36
Q

What is multiple sclerosis?

A

Demyelinating CNS condition.

37
Q

How is MS clinically defined?

A

Two episodes of neurological dysfunction (brain, spinal cord or optic nerves) separated in space and time.

38
Q

Who is MS most likely to present in?

A

White women aged 20-40 years.

39
Q

What is the pathogenesis of the inflammatory phase of MS?

A

Lymphocytes (T-cells) with encephalitogenic potential are activated in the periphery.
Enter into the CNS via attachment to a receptor on endothelial cells.
Inflammatory cytokines released and cause direct toxicity.
Attract macrophages that contribute to demyelination.

40
Q

What is the pathogenesis of the degenerative phase of MS?

A

Reflects axonal degeneration and loss.
Demyelination disrupts axonal support and leads to destabilisation of axonal membrane potentials.
Inflammatory cells, antibodies, and complement may contribute to axonal injury.
Multifocal areas of demyelination, loss of oligodendrocytes, and astrogliosis with loss of axons primarily in the white matter of the CNS.

41
Q

What should be looked for on examination of a patient with MS?

A

Fundoscopy to view optic disc.
Swinging flashlight test to evaluate afferent pupillary defect.
Colour vision to assess for red desaturation.
Eye movements may reveal internucclear ophthalmoplegia
Upper motor neuron signs e.g. spasticity and hyper reflexia

42
Q

What are the investigations of MS?

A

MRI head and spine
Check for thyroid disease, vitamin B12 deficiency and diabetes mellitus.
Lumbar puncture with CSF examination for oligoclonal bands, and CSF IgG index may be done (normal in 10-20% of MS cases)
If MRI is contraindicated, evoked potentials.

43
Q

How are MS relapses treated?

A

High dose methylprednisolone and oral taper.

44
Q

What are the disease modifying therapies for MS?

A

Recommended for patients with a first clinical episode and MRI features consistent with MS or relapsing-remitting.
- Interferon beta-1b and interferon beta-1a

45
Q

What is the management of MS in progressive disease?

A

Ocrelizumab

46
Q

What is the management of symptom control in MS?

A 
Gait - progressive resistance training. 
Fatigue - regular exercise, check bloods, sleep history
Sensory symptoms - gabapentin
Spasticity - baclofen, clonazepam
Urine dysfunction - oxybutynin
Tremor - primidone

Phase 4 (12 decks)

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