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Neuromedicine dr saad
- 15. Mechanisms of drugaction in Parkinson's disease. ( 1) Decarboxylase inhibitors (carbidopa and benserazide) decrease side-effects by reducing peripheral conversion of levodopa to dopamine by aromatic amino acid decarboxylase (AAAD). 2) (2) Active transport of levodopa into the brain may be inhibited by competition from dietary amino acids after a high-protein meal. 3) (3) In the nigrostriatal neurons, levodopa is converted into dopamine. 4) (4) Amantadine enhances the release of dopamine at the nerve terminal. 5) (5) Dopamine agonists act directly on striatal receptors. 6) (6) The monoamine oxidase type B (MAO-B) inhibitor selegiline increases the availability of neuronal dopamine by reducing its metabolism outside the neuron. 7) (7) The catechol-O-methyl-transferase (COMT) inhibitor entacapone prolongs the availability of dopamine by inhibiting the metabolism of dopamine and levodopa outside the neuron
- 23. Hemifacial spasm This usuallypresents after middle age with intermittent twitching around one eye, spreading ipsilaterally to other facial muscles. The spasms are exacerbated by talking, eating and stress. Hemifacial spasm is usually idiopathic (similarly to trigeminal neuralgia, it has been suggested that it is due to an aberrant arterial loop irritating the 7th nerve just outside the pons), but may be symptomatic and secondary to structural lesions or MS. Drug treatment is not effective but injections of botulinum toxin into affected muscles help, although these usually have to be repeated every 3 months or so. In refractory cases, microvascular decompression may be considered.
- 28. Guillain–Barré syndrome Guillain–Barré syndrome(GBS) is a heterogeneous group of immune-mediated conditions with an incidence Ithe most common variant is an acute inflammatorydemyelinating polyneuropathy (AIDP). Axonalvariants, either motor (acute motor axonal neuropathy, AMAN) or sensorimotor (acute motor and sensoryaxonal neuropathy, AMSAN), (often associated with Campylobacter jejuni). The hallmark is an acute paralysis evolving over days or weeks with loss of tendon reflexes. About two-thirds of those with AIDP have a prior history of infection, and autoimmune response triggered by the preceding infection causes demyelination. A number of GBS variantshave been described, associated with specific anti-ganglioside antibodies; the best-recognised isMiller Fisher syndrome, which involves anti-GQ1b antibodies
- 29. Clinical features Distal paraesthesiaand limb pains (often severe) precede a rapidly ascending muscle weakness, from lower to upper limbs, more marked proximally than distally. Facial and bulbar weakness commonly develops, and respiratory weakness requiring ventilatory support occurs in 20% of cases. most patients, weakness progresses for 1-3 weeks, but rapid deterioration to respiratory failure can develop within hours. On examination there is diffuse weakness with widespread loss of reflexes.
- 30. An unusual axonalvariant described by Miller Fisher comprises the triad of ophthalmoplegia, ataxia and areflexia. Overall, 80% of patients recover completely within 3-6 months, 4% die, Adverse prognostic features include older age, rapid deterioration to ventilation and evidence of axonal loss on EMG.
- 31. Investigations The CSF proteinis elevated at some stage of the illness but may be normal in the first 10 days. There is usually no rise in CSF cell number (a lymphocytosis of > 50 × 106 cells/L suggests an alternative diagnosis). Electrophysiological studies are often normal in the early stages but show typical changes after a week or so, with conduction block and multifocal motor slowing, sometimes most evident proximally as delayed F-waves Investigation to identify an underlying cause, such as cytomegalovirus, mycoplasma or Campylobacter, requires a chest X-ray, stool culture and appropriate immunological blood tests. Antibodies to the ganglioside GQ1b are found in the Miller Fisher variant. Acute porphyria ( should be excluded by urinary porphyrin estimation, and serum lead should be measured if there are only motor signs.
- 32. Management During the phaseof deterioration, regular monitoring of respiratory function (vital capacity and arterial blood gases) is required, as respiratory failure may develop with little warning and require ventilatory support. Ventilation may be needed if the vital capacity falls below 1 L, but intubation is more often required because of bulbar incompetence leading to aspiration. General management to protect the airway and prevent pressure sores and venous thrombosis is essential. Corticosteroid therapy has been shown by RCT to be ineffective. However, plasma exchange and intravenous immunoglobulin therapy shorten the duration of ventilation and improve prognosis, provided treatment is started within 14 days of the onset of symptoms