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E. Bram, M.A., M.D., M.P.H.

Associate Professor, Idaho College of Osteopathic Medicine

It may begin unilaterally but both eyes are usually soon affected (Malinovsky 1987). Repeated contractions of the orbicularis oculi can progress to almost constant involuntary spasm, sometimes rendering the patient virtually unable to see. Spasms are provoked by bright light, embarrassment, attempts at reading or looking upward. Some patients fi nd tricks that help: yawning, humming, touching the eyelids or eyebrows, neck extension or forced jaw opening. It is most common in middle-aged or elderly women, with onset particularly in the sixth decade. For some considerable time, even years, it may be intermittent, and the aggravation by emotional influences may give a strong impression that psychological factors are operative. A considerable proportion of patients show depression around the time of onset (Marsden 1976a). The affected patients are typically stable, however, and without precipitants that could explain the disorder (Bender 1969). Oromandibular dystonia has a similar range of onset and also more frequently affects women than men. Prolonged spasms affect the muscles of the mouth, jaw and sometimes the tongue (lingual dystonia). The jaw may be forced open or abruptly closed, the lips purse or retract, and the tongue protrudes or curls within the mouth. The picture can at first sight resemble the orofacial dyskinesias seen as a late effect of neuroleptic medication (see Tardive dyskinesia, under Drug-induced disorders/ Clinical pictures, earlier) but in essence the movements are different (Marsden 1976a,b). Orofacial dystonia consists of repetitive prolonged spasms rather than the incessant flow of choreiform lip smacking, chewing and tongue rolling movements seen in tardive dyskinesia. The spasms are typically provoked by embarrassment, fatigue or attempts at speaking, chewing or swallowing. Certain tricks may be learned to abort them, such as grasping the lower jaw firmly or shaking the head. While each of these two disorders can be seen in isolation, there is a strong tendency for them to be coupled together. In a later series of 264 patients with blepharospasm, 188 (71%) also showed oromandibular dystonia (Grandas et al. When both are present they usually begin contemporaneously, although sometimes the blepharospasm antedates the oromandibular dystonia by several years. Ben Simon and McCann (2005) suggest that isolated blepharospasm occurs only in a minority of patients. Most have a combination of blepharospasm with oromandibular dystonia or a segmental cranial dystonia. Patients may also exhibit frowning, torticollis titubation, or hyperexcitable trigeminal reflex blinks (Mauriello et al. The course is usually chronic and protracted, but can be intermittent over many years. Aetiology the aetiology of both conditions remains obscure, but they are now firmly included within the dystonia spectrum. Blepharospasm was formerly often considered to be psychological in origin, but its frequent association with oromandibular dystonia has served to dispel this view. Functional neuroimaging has demonstrated increased metabolism in the thalamus and striatum (EsmaeliGutstein et al. Several authors focus on basal ganglia abnormalities as the cause of blepharospasm (Berardelli et al. Continuous chronic blepharospasm has also been reported after head injury or subarachnoid haemorrhage, or in association with cerebral tumours, degenerative conditions or cerebral arterial disease. Rostral midbrain lesions appear to be particularly closely related to its development (Poewe et al. In all such settings blepharospasm can sometimes resemble a psychogenic disorder but for the history and abnormal findings on neurological examination.

While in hospital he showed two episodes of elation lasting for several days, the second being frankly manic with pressure of speech, flight of ideas and possibly auditory hallucinations. It was concluded that the thalamic infarctions had led, via diaschisis, to metabolic hypofunction in the frontal lobes, resulting in the abrupt onset of cyclical mood disorder accompanied by features of frontal lobe dysfunction. Three patients were described who were admitted to hospital with supposed major depression, exhibiting severe psychomotor retardation, weight loss, exhaustion and selfreproach. The shared clinical feature was abrupt improvement under hospital care, with relapse to extreme lack of initiative and energy on discharge to the home environment. Such cycles were followed repeatedly, with the patients neglecting to eat or drink and spending most of their time at home in bed. It was suggested that this may represent a specific syndrome of extreme abulia. Milder forms of apathy are quite common after stroke, and though they are usually observed in patients who are also depressed, may be seen in isolation (Starkstein et al. The most thorough study of the incidence of delusional ideas rated 360 patients admitted within 1 day of stroke every day while they were in hospital (Kumral & Ozturk 2004). Delusional ideation was found in 15 patients (4%), with onset within a few days of stroke. All patients were treated with haloperidol or quetiapine and the delusions lasted on average 13 days, tending to ameliorate alongside the other behavioural problems. It was therefore not surprising to find that in four cases there was Capgras delusion, and one other case of delusional misidentification. These findings are very much in line with Price and Mesulam (1985), who described five cases of delusions occurring in the acute phase after stroke, all with right hemisphere lesions. Levine and Finklestein (1982) have also noted an apparent relationship between cerebrovascular lesions of the right hemisphere, specifically of the right temporoparieto-occipital areas, and the development of psychotic illnesses some time later. Eight patients were described, with the psychoses Cerebrovascular Disorders 489 appearing some weeks or years after the stroke. All but one had developed seizures in the interim, which may have been a connecting factor. The psychoses developed acutely, with formed auditory and visual hallucinations; the majority of patients showed agitation, persecutory delusions and confusion, but in some the hallucinatory phenomena were relatively pure. All had constructional apraxia, and most showed a variety of other neurological residua. The right-sided location in every case may have reflected the freedom from dysphasia, allowing the psychoses to be revealed, or alternatively may have reflected the predisposing effects of spatial disabilities in leading to environmental misinterpretations. The combination of right hemisphere infarcts with poststroke seizures as a risk for psychosis has been found in a further five cases (Rabins et al. Hallucinosis, in which the patient retains insight into the unreal nature of the hallucinated material, has traditionally been related to lesions in the midbrain and pons, the peduncular hallucinosis of Lhermitte (1922, 1932) described in Chapter 1 (Basic concepts and terminology/Organic hallucinosis). Such hallucinosis can occur in the visual or auditory modalities, is typically complex and vivid, and usually resolves within days or weeks. On the other hand, hallucinations may be seen after cortical strokes; 4 of 641 patients had auditory hallucinations in the early poststroke period and in all cases the lesion was in the right temporal lobe (Lampl et al. Given the concern that antipsychotics, when used to treat psychosis in the elderly, may be associated with an increased risk of stroke, care is required when prescribing these agents to patients who have suffered a stroke. If antipsychotics are to be prescribed, any potential risks should be discussed with the patient and the family. As noted above, targeted treatments during this period are aimed at promoting survival of cells in the penumbra. However, numerous less specific matters need to be addressed that can all be considered under the rubric of rehabilitation. Nursing and therapy will minimise secondary complications such as bed sores, contractures and subluxation of joints. As soon as feasible more specific rehabilitation will be available, early on relying heavily on physiotherapy (Young & Forster 2007). It is possible that such early rehabilitation interventions can influence neuroplastic change such that there is transfer of lost functions to unaffected brain areas, and reorganisation within the brain to allow other areas to contribute more. There is good evidence that physiotherapy is helpful, particularly in terms of exercise training to improve balance and gait. However, attempts to demonstrate the value of physiotherapy in improving limb function, as in hemiparetic stroke, have been less successful.

Syndromes

• Genetic testing for change (mutation) in the iduronate sulfatase gene
• X-rays of the spine and pelvis
• Sore and tender tongue
• An implant may be placed underneath the chest wall muscles to help match the size of your other breast.
• Medicine (antidote) to reverse the effect of the poison (fomepizole or ethanol)
• Urinalysis. This test is done to look for white blood cells, red blood cells, bacteria, and to test chemicals, such as nitrites in the urine. This test can diagnose an infection most of the time.
• Go to the dentist every year for an exam and cleaning.
• Prescription medicine that you apply at home several times per week
• Shortness of breath