Ch 11 Neurovascular & Neurotoxicology Flashcards
(30 cards)
What is PRES?
Posterior reversible encephalopathy syndrome - characterised by widespread vasogenic oedema worse in the parietal and occipital lobes (watershed area)
What conditions are associated with PRES?
Hypertension, pre-eclampsia/eclampsia, sepsis, shock, autoimmune disease, chemotherapy and transplantation.
How is PRES treated?
Control of the underlying cause and tight BP management.
What is crossed cerebellar diaschisis?
Degeneration of the contralateral cerebellum secondary to a cerebral hemispheric lesion. The mechanism is due to a reduction in cerebral blood flow and hypometabolism.
What is Giant cell arteritis?
Aka temporal arteritis, characterised by chronic granulomatous arteritis with skip lesions. If untreated may lead to blindness. M:F = 1:2.
What is the management of Giant cell arteritis?
High dose steroids 40mg Prednisolone BD (do not withhold steroids whilst waiting for biopsy!) and temporal artery biopsy.
What is the distinguishing factor between Tayayasu’s arteritis and GCA?
Young women and large arteries more effected. Has an inflammatory phase followed by a stenotic phase.
What condition is associated with GCA?
50% have polymyalgia rheumatica
What are the clinical features of GCA?
Headache, scalp tenderness, jaw claudication, blindness / VF defect. Associated with polyneuropathies and thoracic aortic aneurysms (17x more likely with GCA!)
What investigations would you perform for a patient with suspected GCA?
FBC
ESR / CRP (CRP more sensitive)
Rheumatiod factor, ANA and complement (should be negative, otherwise think of another diagnosis!)
Temporal artery biopsy
(angiography if suspicion of large artery involvement exists)
How is a temporal artery biopsy performed?
GA, informed consent Mark the frontal branch of the STA LA Incision behind the hairline and parallel to the artery STA is supfl to the temporalis fascia 5 cm length dissected
What is PMR?
Inflammatory condition of unknown cause characterised by shoulder, neck and hip pain. ESR raised. Responds to low dose steroids. Risk of GCA.
What are the ANCA-vasculitides?
Wegener’s granulomatosis (C-ANCA +)
Churg-strauss (P-ANCA +)
Polyarteritis nodosa
What is fibromuscular dysplasia (don’t confuse this with fibrous dysplasia!)?
Vasculopathy primarily affecting the renal arteries and internal carotid. Assoc with hypertension. Causes multifocal arterial constriction with intervening aneurysmal dilatations - ‘string of pearls’ sign.
What % of patients with FMD have aneurysms?
20-50%
How is fibromuscular dysplasia diagnosed?
Angiogram! Treat with aspirin.
What is CADASIL?
Cerebral autosomal dominant arteriopathy and subcortical infarcts with leukoencephalopathy. Due to vasculopathy of leptomeningeal and perforating arteries.
What is Eaton-Lambert syndrome?
Paraneoplastic syndrome with Ab to presynaptic Ca channels therefore preventing Ach release into the NMJ. Worse in the morning and improves through the day (c.f. with myaesthenia gravis)
What are the effects of ETOH on the nervous system?
Acute - trauma, withdrawl, DTs, Seizures
Chronic - CPM, hypoNa, Thiamine deficiency, Peripheral neuropathies, Wernicke’s encephalopathy / Korsakoff’s.
How is ETOH withdrawl managed?
Tapering doses of benzo (Chlordiazepoxide)
Thiamine, B12 and Folate (Pabrinex) should also be given.
What is the triad of Wernicke’s encephalopathy?
Encephalopathy, ophthalmoplegia (horizontal nystagmus) and gait ataxia (cerebellar and vestibular impairment)
What causes Wernicke’s encephalopathy?
Thiamine deficiency
What are the MRI findings in Wernicke’s encephalopathy?
High T2 / FLAIR signal in the medial thalamus, floor of the 4th ventricle and periaqueductal GM. Atrophy of the mammillary bodies.
What is the treatment of Wernicke’s encephalopathy?
100 mg Thiamine IV (before giving any IV glucose!)
