Neurology Flashcards

Question

What is the pathogenesis of delirium?

Answer 1

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.

Answer 2

Hyperactive | Hypoactive

Answer 3

``` 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 ```

Answer 4

``` Immobility Use of physical restraint Use of bladder catheter Iatrogenic events Malnutrition Psychoactive medications Intercurrent illness Dehydration ```

Answer 5

``` Dementia Depression Mania Schizophrenia Dysphasia Non convulsive epilepsy/temporal lobe epilepsy Hepatic encephalopathy ```

Answer 6

``` 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 ```

Answer 7

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.

Answer 8

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

Answer 9

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

Answer 10

``` Re bleeding Acute hydrocephalus Vasospasm Venricular wall motion abnormalities Pulmonary oedema Seizures Cognitive impairment ```

Answer 11

1 in 4 dead at 6 months.

Answer 12

Demyelinating CNS condition.

Answer 13

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

Answer 14

White women aged 20-40 years.

Answer 15

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.

Answer 16

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.

Answer 17

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

Answer 18

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.

Answer 19

High dose methylprednisolone and oral taper.

Answer 20

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

Answer 21

Ocrelizumab

Answer 22

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