Neuro Flashcards

1
Q

Name the 6 main types of peripheral nerve damage

A

Demyelination (eg Guillan-Barre syndrome)
Axonal degeneration (eg toxic neuropathies)
Wallerian degeneration (both axon and myelin sheath degenerates)
Compression (entrapment neuropathies, eg carpal tunnel)
Infarction (microinfarction of vasa nervorum occurs in diabetes and arteritis)
Infiltration (infiltration of peripheral nerves by inflammatory cells - leprosy, granulomas, mets)

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2
Q

Name common risk factors for stroke /TIA

A

Hypertension, smoking, DM, heart disease, PVD, post-TIA, carotid artery occlusion, excess alcohol, clotting disorders, hyperlipidaemia

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3
Q

How does nerve regeneration occur?

A

Limited

Remyelination and axonal growth (~1mm/day)

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4
Q

Pathology of epilepsy?

A

Patients’ “seizure threshold” is lowered, meaning that the level of excitability at which cells will discharge uncontrollably is lower.
Neurons are HYPEREXCITABLE

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5
Q

Common things that push neuron excitability past the seizure threshold in epilepsy?

A

Sleep deprivation, alcohol, drugs, physical exhaustion, flickering lights, infection/metabolic disturbance,
Etc

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6
Q

Most common causes of peripheral neuropathy?

A
Diabetes
Alcoholism
Vitamin deficiency (B12)
Infected / inherited (guillan-barre, Charcot-Marie-tooth)
Drugs - eg isoniazid
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7
Q

What happens in a simple partial seizure?

A

Patient remains conscious
Focal motor seizure - jerking usually begins at corner of mouth/in one hand and sometimes spreads to involve entire side.

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8
Q

What happens in a complex partial seizure?

A

TEMPORAL LOBE SEIZURE
Impaired consciousness
Deja vu, jamais vu, vertigo, visual/auditory hallucinations, lip smacking/other motor disturbances, tachycardia, emotional disturbance, automatism (patient literally goes on autopilot and can wander off somewhere)
Drowsiness and confusion after attack

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9
Q

Difference between absence seizure and temporal lobe/complex partial seizure?

A

Absence = quicker recovery after the attack

Absence generally lasts 30s

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10
Q

What is status epilepticus?

A

A seizure that lasts >30 minutes
OR
Multiple seizures in between which consciousness is not recovered, lasting >30 minutes
MEDICAL EMERGENCY

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11
Q

How is status epilepticus treated?

A

Benzodiazepines (IV or IM)
2nd line - phenobarbital
3rd line - phenytoin

(+RRAPID)

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12
Q

Mechanism of carbamazepine? (Anti-epileptic)

A

Inhibits sodium channels
➡️reducing action potential propagation of neurons

Phenytoin has the same mechanism!

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13
Q

Mechanism of sodium valproate?

A

Increases GABA concentration
Inhibits sodium channels
Inhibits glutamate decarboxylase

First line for absence & generalised seizures, second line for partial

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14
Q

Triad of symptoms for meningitis?

A

Headache
Neck stiffness
Fever

Pretechial/non blanching rash - medical emergency!! Beware of septicaemic shock

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15
Q

Other symptoms/signs for meningitis, besides the triad?

A

(Triad = headache, stiff neck, fever)

Pretechial/non blanching rash - medical emergency!! Beware of septicaemic shock
Photophobia
Vomiting
Malaise, rigors
Positive Kernigs sign
Conscious but delirious in high fever
Focal signs may be present eg papilloedema, Diplopia.

Viral may be less prominent signs

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16
Q

Headache red flags?

Indicative of tumour

A

Papilloedema
New seizure
Headache with other significant conditions eg malignancy (especially lung or breast)
abnormal neuro signs - altered consciousness, confusion, lack of coordination…

17
Q

Main features of tension headache?

A
Tight band sensations 
Pressure behind eyes
Throbbing/bursting sensations
Precipitating factors - worry, noise, concentrated visual effort, fumes
Depression
Analgesia overuse
18
Q

Difference between Parkinson’s disease and Parkinsonism?

A

PD = idiopathic syndrome of Parkinsonism

-ism = drug induced, encephalitis/toxin related giving Parkinson symptoms

19
Q

Mechanism of Parkinson’s disease?

A

Progressive neuronal degeneration of the pars compacta in the substantia nigra - leading to development of Lewy bodies containing protein filaments.
+ degeneration of basal ganglia nuclei
This gives a loss of dopamine (and melanin) in the striatum.
Amount lost correlates with cell loss and degree of akinesia