Cases reported "Hemiplegia"

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1/8. hemiplegia hypoglycaemia syndrome.

    We report the case of a 83-year-old man who presented to the emergency department with hypoglycaemia resembling a cerebrovascular accident. Hypoglycaemic hemiparesis is an under-recognized manifestation of hypoglycaemia. If not recognized and treated promptly, hypoglycaemia may cause irreversible central nervous system injury; it rarely results in death. It is imperative that emergency physicians consider hypoglycaemia in all patients with coma in spite of focal neurological deficit even when the findings seem to be explained initially by other aetiologies.
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2/8. neurologic manifestations of cerebral air embolism as a complication of central venous catheterization.

    OBJECTIVE, patients, AND methods: A severe case of cerebral air embolism after unintentional central venous catheter disconnection was the impetus for a systematic literature review (1975-1998) of the clinical features of 26 patients (including our patient) with cerebral air embolism resulting from central venous catheter complications. RESULTS: The jugular vein had been punctured in eight patients and the subclavian vein, in 12 patients. embolism occurred in four patients during insertion, in 14 patients during unintentional disconnection, and in eight patients after removal and other procedures. The total mortality rate was 23%. Two types of neurologic manifestations may be distinguished: group A (n = 14) presented with encephalopathic features leading to a high mortality rate (36%); and group B (n = 12) presented with focal cerebral lesions resulting in hemiparesis or hemianopia affecting mostly the right hemisphere, with a mortality rate as high as 8%. In 75% of patients, an early computed tomography indicated air bubbles, proving cerebral air embolism. Hyperbaric oxygen therapy was performed in only three patients (12%). A cardiac defect, such as a patent foramen ovale was considered the route of right to left shunting in 6 of 15 patients (40%). More often, a pulmonary shunt was assumed (9 of 15 patients; 60%). For the remainder, data were not available. CONCLUSION: When caring for critically ill patients needing central venous catheterization, nursing staff and physicians should be aware of this potentially lethal complication.
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3/8. motor cortex stimulation for central pain following a traumatic brain injury.

    Central pain can occur in any lesions along the central nervous system affecting the spinothalamocortical pathway. Although diverse etiologies have been reported to cause central pain, there are few reports on the occurrence and surgical treatment of central pain following a traumatic brain injury (TBI). This paper describes the occurrence of central pain following a severe TBI, in which the diagnosis of central pain was typically delayed due to the patient's decreased ability to express his pain for severe aphasia as a neurological sequela. The severe burning pain, deep pressure-like pain, and deep mechanical allodynia, which presented over the contralateral side to the TBI, were successfully relieved with motor cortex stimulation (MCS). The analgesic effect of stimulation was found to be long lasting and was still present at the 12-month follow up. As shown in this patient, the occurrence of central pain syndrome should be considered by physicians caring for TBI patients, and a comprehensive, systematic study will be needed to determine the prevalence of central pain after a TBI.
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4/8. Hemiatrophy and hemiparesis in a patient with congenital cytomegalovirus infection.

    A 3-year-old girl with congenital cytomegalovirus (CMV) infection has been followed up since birth. Hemiatrophy and hemiparesis occurred at 9 months of age. These unusual sequels of congenital CMV infection should encourage physicians to do longitudinal studies on infants with congenital CMV infection, as well as to examine children with hemiatrophy and hemiparesis for CMV infection.
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5/8. Nonhemorrhagic pontine infarct in a child following mild head trauma.

    A child who presented with hemiparesis secondary to a delayed non-hemorrhagic pontine infarction following mild head trauma is described. The results of the child's workup, including computed tomography (CT), were negative. The diagnosis of nonhemorrhagic pontine infarct was made by magnetic resonance imaging (MRI). The diagnostic evaluation excluded other possible etiologies of cerebral infarction, including vasculitides, CNS infection, congenital heart disease, hypercoagulable states, and demyelinating diseases. Although trauma cannot be proven as the cause of the infarct, other known causes of infarct were excluded. There are few cases of traumatic nonhemorrhagic cerebral infarction among children in the literature; none describes diagnostic MRI findings. MRI is important in these cases, because it may reveal delayed infarction from small-vessel injury, which is not apparent on CT. This article discusses the etiology of and the diagnostic evaluation of pediatric cerebrovascular accidents and suggests the need for emergency physicians to consider trauma as a potential cause of delayed nonhemorrhagic cerebral infarct in children.
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6/8. Mute postseizure patient: an unusual manifestation of Todd's phenomenon.

    patients who manifest neurologic deficits after a seizure can present an interesting challenge to emergency physicians, particularly when the deficits are not those normally associated with Todd's phenomenon. Although Todd's phenomenon is known to result in a wide variety of transient focal deficits, we find no case report in the medical literature of this entity resulting in mutism. We present a case of a 51-year-old woman with transient mutism and hemiparesis caused by Todd's phenomenon. We also review some of the neuroanatomic and neurophysiologic issues relating to the etiology of Todd's phenomenon, as well as alternative management strategies.
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7/8. Accidental penetrating cervical cord injury in a young child.

    A three-year-old child presented to our emergency department with a hemiparesis five days following the accidental laceration of her neck with a piece of glass. The laceration had been thought to be superficial when she was initially evaluated. When seen again three days following the injury because of right-sided weakness, computerized tomography of her head and neck was unrevealing. However, using high resolution magnetic resonance imaging (MRI) we were able to demonstrate a C1-2 cord contusion and an injury tract leading from the surface of the neck to this site. The unusual mechanism of injury and the underlying pathophysiology of this patient's presentation are reviewed. It is important for the emergency physician to be reminded that what appears to be a superficial laceration can sometimes be more serious. MRI should be considered in the evaluation of patients who have suffered penetrating trauma if the potential for spinal cord injury exists and especially when there are signs or symptoms suggesting spinal cord dysfunction.
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8/8. The functional anatomy of a hysterical paralysis.

    The concept of a conversion disorder (such as hysterical paralysis) has always been controversial (Ron, M.A. (1996). Somatization and conversion disorders. In: B.S. Fogel, R.B. Schiffer & S.M. Rao (Eds.), neuropsychiatry. Williams and Wilkins, baltimore, MD). Although the diagnosis is recognised by current psychiatric taxonomies, many physicians still regard such disorders either as feigned or as failure to find the responsible organic cause for the patient's symptoms. We report a woman with left sided paralysis (and without somatosensory loss) in whom no organic disease or structural lesion could be found. By contrast, psychological trauma was associated with the onset and recurrent exacerbation of her hemiparalysis. We recorded brain activity when the patient prepared to move and tried to move her paralysed (left) leg and when she prepared to move and did move her good (right) leg. Preparing to move or moving her good leg, and also preparing to move her paralysed leg, activated motor and/or premotor areas previously described with movement preparation and execution. The attempt to move the paralysed leg failed to activate right primary motor cortex. Instead, the right orbito-frontal and right anterior cingulate cortex were significantly activated. We suggest that these two areas inhibit prefrontal (willed) effects on the right primary motor cortex when the patient tries to move her left leg.
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