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SELECTED NEUROCUTANEOUS DISEASES 1 Tuberous Sclerosis
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Tuberous sclerosis may occur sporadically or on a familial basis with autosomal dominant inheritance The responsible gene is located on the long arm of chromosome 9 in at least some cases Its pathogenesis is unknown Neurologic presentation is with seizures and progressive psychomotor retardation beginning in early childhood The cutaneous abnormality, adenoma sebaceum, becomes manifest usually between 5 and 10 years of age and typically consists of reddened nodules on the face (cheeks, nasolabial folds, sides of the nose, and chin) and sometimes on the forehead and neck Other typical cutaneous lesions include subungual fibromas, shagreen patches (leathery plaques of subepidermal fibrosis, situated usually on the trunk), and leaf-shaped hypopigmented spots Associated abnormalities include retinal lesions and tumors, benign rhabdomyomas of the heart, lung cysts, benign tumors in the viscera, and bone cysts The disease is slowly progressive and leads to increasing mental deterioration There is no specific treatment, but anticonvulsant drugs may help in controlling seizures
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3 Sturge-Weber Syndrome
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Sturge-Weber syndrome consists of a congenital, usually unilateral, cutaneous capillary angioma involving the upper face, leptomeningeal angiomatosis, and, in many patients, choroidal angioma It has no sex predilection and usually occurs sporadically The cutaneous angioma sometimes has a more extensive distribution over the head and neck and is often quite disfiguring, especially if there is associated overgrowth of connective tissue Focal or generalized seizures are the usual neurologic presentation and may commence at any age There may be contralateral homonymous hemianopia, hemiparesis and hemisensory disturbance, ipsilateral glaucoma, and mental subnormality Skull x-rays taken after the first 2 years of life usually reveal gyriform ( tramline ) intracranial calcification, especially in the parieto-occipital region, due to mineral deposition in the cortex beneath the intracranial angioma Treatment is aimed at controlling seizures pharmacologically Ophthalmologic advice should be sought concerning the management of choroidal angioma and of increased intraocular pressure
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MOVEMENT DISORDERS 1 Benign Essential (Familial) Tremor
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has significant morbidity, whereas the risks of bilateral stimulation are appreciably lower
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Louis ED Essential tremor Lancet Neurol 2005 Feb;4(2):100 10 [PMID: 15664542] Ondo WG Essential tremor: treatment options Curr Treat Options Neurol 2006 May;8(3):256 67 [PMID: 16569384] Ondo WG et al Topiramate in essential tremor: a double-blind, placebo-controlled trial Neurology 2006 Mar 14;66(5):672 7 [PMID: 16436648]
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ESSENTIALS OF DIAGNOSIS
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Postural tremor of hands, head, or voice Family history common May improve temporarily with alcohol No abnormal findings other than tremor
2 Parkinsonism
General Considerations
The cause of benign essential tremor is uncertain, but it is sometimes inherited in an autosomal dominant manner Responsible genes have been identified at 3q13 and 2p22-p25
ESSENTIALS OF DIAGNOSIS
Any combination of tremor, rigidity, bradykinesia, progressive postural instability Seborrhea of skin quite common Mild intellectual deterioration may occur
Clinical Findings
A Symptoms and Signs
Tremor may begin at any age and is enhanced by emotional stress The tremor usually involves one or both hands, the head, or the hands and head, while the legs tend to be spared Examination reveals no other abnormalities Ingestion of a small quantity of alcohol commonly provides remarkable but short-lived relief by an unknown mechanism Although the tremor may become more conspicuous with time, it generally leads to little disability Occasionally, it interferes with manual skills and leads to impairment of handwriting Speech may also be affected if the laryngeal muscles are involved
General Considerations
Parkinsonism is a relatively common disorder that occurs in all ethnic groups, with an approximately equal sex distribution The most common variety, idiopathic Parkinson s disease (paralysis agitans), begins most often between 45 and 65 years of age
Etiology
Parkinsonism may rarely occur on a familial basis, and the parkinsonian phenotype may result from mutations of several different genes Postencephalitic parkinsonism is becoming increasingly rare Exposure to certain toxins (eg, manganese dust, carbon disulfide) and severe carbon monoxide poisoning may lead to parkinsonism Typical parkinsonism has occurred in individuals who have taken 1-methyl-4-phenyl1,2,5,6-tetrahydropyridine (MPTP) for recreational purposes This compound is converted in the body to a neurotoxin that selectively destroys dopaminergic neurons in the substantia nigra Reversible parkinsonism may develop in patients receiving neuroleptic drugs (see 25), reserpine, or metoclopramide Only rarely is hemiparkinsonism the presenting feature of a progressive space-occupying lesion In idiopathic parkinsonism, dopamine depletion due to degeneration of the dopaminergic nigrostriatal system leads to an imbalance of dopamine and acetylcholine, which are neurotransmitters normally present in the corpus striatum Treatment is directed at redressing this imbalance by blocking the effect of acetylcholine with anticholinergic drugs or by the administration of levodopa, the precursor of dopamine
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