Handbook of clinical neurology
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Mood disturbances, especially depressive disorders, are the most frequent neuropsychiatric complication of traumatic brain injury (TBI). These disorders have a complex clinical presentation and are highly comorbid with anxiety, substance misuse, and other behavioral alterations such as impulsivity and aggression. Furthermore, once developed, mood disorders tend to have a chronic and refractory course. ⋯ In turn, the onset of mood disorders may contribute to further prefrontal dysfunction among TBI patients. Finally, in spite of the prevalence and impact of these disorders, there have been relatively few rigorous studies of therapeutic options. Development of treatment strategies constitutes a priority in this field of research.
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Child traumatic brain injury (TBI) is a major cause of disability in early life. Unlike in adults, a TBI in childhood causes an insult to a brain that is developing, potentially affecting future brain maturation, neural connectivity, and the acquisition of new skills. This review considers how such early brain insult may impact children's functional abilities, and how these processes may link with differential patterns of recovery across infancy, childhood, and adolescence. ⋯ To assist in understanding what may contribute to outcomes, we discuss predictive factors (injury severity, child and environment status) and research reporting on their individual and combined effect on recovery. The identification of such outcome predicators has led to an emerging literature in the area of intervention and rehabilitation that we also summarize. Finally, it concludes with discussion of the future direction of pediatric TBI research.
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Reversible cerebral vasoconstriction syndrome is characterized by severe headaches with or without focal neurologic deficits and/or seizures, and segmental constriction of cerebral arteries that resolves within 3 months. This increasingly recognized syndrome is supposedly due to a transient disturbance in the control of cerebral vascular tone with sympathetic overactivity. It can cause stroke in the young. ⋯ Convexity subarachnoid hemorrhage or stroke may occur a few days after initial normal imaging, and cerebral vasoconstriction is maximal on angiography 2-3 weeks after clinical onset. Symptomatic treatment includes rest and removal of vasoactive substances. Nimodipine has been proposed to reduce thunderclap headaches within 48 hours, but has no proven effect on the hemorrhagic and ischemic complications.
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Neuropathies related to diabetes mellitus can affect 60-70% of patients with diabetes. These can include peripheral polyneuropathies, mononeuropathies, and autonomic neuropathies. ⋯ Besides control of the above listed risk factors, we do not have effective medications to treat the pathophysiologic mechanisms of diabetic neuropathies. Treatment is limited to ameliorating pain and correcting the end organ consequences of the neuropathic processes.
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Independent of the underlying condition, critical illness is characterized by a uniform dysregulation of the hypothalamic-pituitary-peripheral axes. In most axes a clear biphasic pattern can be distinguished. The acute phase of critical illness is characterized by low peripheral effector hormone levels such as T3, IGF-1 and testosterone, despite an actively secreting pituitary. ⋯ In the prolonged phase of critical illness, low peripheral effector hormone levels coincide with a uniform suppression of the neuroendocrine axes, predominantly of hypothalamic origin. The severity of the alterations in the different neuroendocrine axes is associated with a high risk of morbidity and mortality, but it remains unknown whether the observed changes are cause or consequence of adverse outcome. Several studies have identified therapeutic potential of hypothalamic releasing factors, but clinical outcome remains to be investigated with sufficiently powered randomized controlled trials.