Neurology Flashcards
(176 cards)
Drug side effects:
Peripheral neuropathy
amiodarone phenytoin metronidazole nitrofurantoin isoniazid
Drug side effects:
thrombocytopenia
sodium valproate
heparin
Mechanism of action:
Phenytoin
binds to sodium channels increasing their refractory period
P450 inducer
Phenytoin
Adverse effects
Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures
Phenytoin
Adverse effects
Chronic
gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia
Phenytoin
Adverse effects
Idiosyncratic
fever rashes, including severe reactions such as toxic epidermal necrolysis hepatitis Dupuytren's contracture* aplastic anaemia drug-induced lupus
Phenytoin monitoring
Phenytoin levels do not need to be monitored routinely but trough levels, immediately before dose should be checked if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication
Brain lesions
Gross anatomy
Parietal lobe lesions
sensory inattention apraxias astereognosis (tactile agnosia) inferior homonymous quadrantanopia Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
Brain lesions
Gross anatomy
Occipital lobe lesions
homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia
Brain lesions
Gross anatomy
Temporal lobe lesions
Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
Brain lesions
Gross anatomy
Frontal lobe lesions
expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting disinhibition perseveration anosmia inability to generate a list
Brain lesions
Gross anatomy
Cerebellar lesions
midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
Brain lesions
Medial thalamus and mammillary bodies of the hypothalamus
Wernicke’s and Korsakoff’s
Brain lesions
Subthalamic nucleus of the basal ganglia
Hemiballism (coarse, violent, wide amplitude movements, ipsilateral arm and leg).
Brain lesions
Striatum (caudate nucleus) of the basal ganglia
Huntington’s Chorea
Brain Lesions
Substantia nigra of the basal ganglia
Parkinson’s disease
Brain lesions
Amygdala
Kluver-Bucy syndrome (hypersexuality, hyperorality, hyperphagia, visual agnosia
What is Friedreich’s ataxia?
Friedreich’s ataxia is the most common of the early-onset hereditary ataxias. It is an autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat in the X25 gene on chromosome 9 (frataxin). Friedreich’s ataxia is unusual amongst trinucleotide repeat disorders in not demonstrating the phenomenon of anticipation.
The typical age of onset is 10-15 years old. Gait ataxia and kyphoscoliosis are the most common presenting features.
Neurological features of Friedreich’s ataxia
absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration
Other features of Friedreich’s ataxia
hypertrophic obstructive cardiomyopathy (90%, most common cause of death) diabetes mellitus (10-20%) high-arched palate
uses of carbamazepine
focal seizures - epilepsy
trigeminal neuralgia
bipolar disordre
Mechanism of action - carbamazepine
binds to sodium channels to increase their refractory period
Side effects of carbamazepine
P450 enzyme inducer dizziness and ataxia drowsiness headache visual disturbances (especially diplopia) Steven-Johnson syndrome leucopenia and agranulocytosis hyponatraemia secondary to syndrome of inappropriate ADH secretion
Carbamazepine is known to exhibit autoinduction, hence when patients start carbamazepine they may see a return of seizures after 3-4 weeks of treatment.
Stroke symptoms
anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper