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Care of the delirious and confused patient is of the utmost importance It has been estimated that 20 to 25 percent of medically ill hospital inpatients will experience some degree of confusion; moreover, elderly patients who are delirious have a signi cant level of mortality, variously estimated at 22 to 76 percent (Weber) Optimal care begins with the identi cation of individuals at risk for delirium, including those who have an underlying dementia, pre-existing medical illnesses, or a history of alcohol abuse or depression Further, delirium is more common in males and, not surprisingly, is more likely when sensory function is already impaired (loss of vision and hearing) (Burns, Weber) The primary therapeutic effort is directed to the control of the underlying medical disease and discontinuing offending drugs or toxic agents Other important objectives are to quiet the agitated patient and protect him from injury.

nated as de ciency amblyopia or nutritional optic neuropathy (Chap 41) The same disorder may be seen under conditions of severe dietary deprivation (Strachan syndrome, page 992) and in patients with vitamin B12 de ciency (page 994) Another cause is Leber hereditary optic atrophy, an inherited disorder of mitochondria, a subject that is reviewed by Newman and discussed in Chap 37 Subacute optic neuropathy of possible toxic origin has been described in Jamaican natives It is characterized by a bilaterally symmetrical central visual loss and may have additional features of nerve deafness, ataxia, and spasticity A similar condition has been described in other Caribbean countries, most recently in Cuba, where an optic neuropathy of epidemic proportions was associated with a sensory polyneuropathy.

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A nurse, attendant, or member of the family should be with such a patient at all times if this can be arranged A room with adequate natural lighting will aid in creating a diurnal rhythm of activity and reduce sundowning It is often better to let an agitated patient walk about the room than to tie him in bed, which may increase his fright or excitement and cause him to struggle to the point of exhaustion and collapse The less active patient can be kept in bed by side rails, wrist restraints, or a restraining sheet or vest The fully awake but confused patient should be permitted to sit up or walk about the room part of the day unless this is contraindicated by the primary disease All drugs that could possibly be responsible for the acute confusional state or delirium should be discontinued if this can be done safely.

These de cits are also demonstrated most clearly in the parkinsonian patient. The prevailing posture is one of involuntary exion of the trunk and limbs and of the neck. The inability of the patient to make appropriate postural adjustments to tilting or falling and his inability to move from the reclining to the standing position are closely related phenomena. A gentle push on the patient s sternum or back may cause a fall or start a series of small corrective steps that the patient cannot control (festination). These postural abnormalities are not attributable to weakness or to defects in proprioceptive, labyrinthine, or visual function, the principal forces that control the normal posture of the head and trunk. Anticipatory and compensatory righting re exes are also manifestly impaired. This occurs early in the course of progressive supranuclear palsy and later in Parkinson disease. A point of interest is whether akinesia and disorders of postural xation are invariable negative manifestations of all extrapyramidal diseases and whether, without them, there could be any secondary release effects such as dystonia, choreoathetosis, and rigidity. The question has no clear answer. Akinesia and abnormalities of posture are constant features of both Parkinson and Wilson diseases; they seem to be present also in Huntington chorea and in the athetosis of cerebral palsy, but one cannot be sure of their existence in hemiballismus.

These include sedating, antianxiety, narcotic, anticholinergic, antispasticity, and corticosteroid medications, L-dopa, metoclopramide (Reglan), and cimetidine (Tagamet) as well as antidepressants, antiarrhythmics, anticonvulsants, and antibiotics Despite the need to be sparing with medications in these circumstances, haloperidol, quetiapine, and risperidone are helpful in calming the agitated and hallucinating patient, but they too should.

A nutritional etiology, rather than tobacco use (putatively, cigars in the Cuban epidemic), is likely but has not been proved conclusively (see Sadun et al and the Cuba Neuropathy Field Investigation report) Impairment of vision due to methyl alcohol intoxication (methanol) is abrupt in onset and characterized by large symmetrical central scotomas as well as symptoms of systemic disease and acidosis Treatment is directed mainly to correction of the acidosis The subacute development of central eld defects has also been attributed to other toxins and to the chronic administration of certain therapeutic agents: halogenated hydroxyquinolines (clioquinol), chloramphenicol, ethambutol, isoniazid, streptomycin, chlorpropamide (Diabinese), in ixamab, and various ergot preparations The main drugs reported to have a toxic effect on the optic nerves are listed in Table 13-3 and have been catalogued by Grant.

Figure 7-9

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