Journal of neurosurgery
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Journal of neurosurgery · Dec 1998
Case ReportsThiamine-deficient lactic acidosis with brain tumor treatment. Report of three cases.
Lactic acidosis due to thiamine deficiency is known to complicate chemotherapy and radiotherapy treatment of malignant extracranial tumors, but to the authors' knowledge, this complication has not been reported in patients treated for malignant brain tumors. They report three such cases, demonstrating that this complication can occur during treatment of brain tumors. In all patients, consciousness levels deteriorated within 1 to 2 days. ⋯ Demand for thiamine is thought to be increased in patients with malignant brain tumors, and supplemental thiamine during treatment is necessary to prevent lactic acidosis. When this complication occurs, immediate treatment with sufficient thiamine is essential, together with normalization of pH by using sodium bicarbonate. With timely intervention, the level of consciousness can recover to the preacidotic state with no new neurological deficits.
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Journal of neurosurgery · Dec 1998
Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study.
To determine the extent and duration of change in extracellular glutamate levels after human traumatic brain injury (TBI), 17 severely brain injured adults underwent implantation of a cerebral microdialysis probe and systematic sampling was conducted for 1 to 9 days postinjury. ⋯ Extracellular neurochemical measurements of excitatory amino acids may provide a marker for secondary insults that can compound human TBI.
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Journal of neurosurgery · Dec 1998
Case ReportsEvidence for end-to-side sensory nerve regeneration in a human. Case report.
Division of a peripheral nerve produces an axotomy leading to neurite outgrowth from the proximal stump and wallerian degeneration in the distal stump. Because there is no longer a connection between the distal stump and neuronal cell bodies in the anterior spinal cord or dorsal root ganglion, it is assumed that no neurites should exist in the distal stump. The authors present the case of a patient who unexpectedly had a neuroma on the proximal end of the distal segment of a previously severed nerve. ⋯ Our hypothesis is that the proximal end of the distal portion of a severed nerve may be innervated by collateral sprouts of axons that branch at points of more distal plexus formation. This invokes a similar pathophysiology to the controversial notion of end-to-side nerve sprouting. Neuromas that develop on the "wrong side" of a nerve become an additional potential source of pain in patients with injured nerves.
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Journal of neurosurgery · Dec 1998
Case ReportsMicrovascular decompression for superior oblique myokymia: first experience. Case report.
Superior oblique myokymia (SOM) is a rare eye movement disorder presenting as uniocular rotatory microtremor due to intermittent contractions of the superior oblique muscle. Medical treatment usually fails to provide long-term benefit for the patient and has considerable side effects. Surgical alternatives including tenotomy or partial tenectomy of the superior oblique tendon often result in incomplete resolution of the visual symptoms. ⋯ There was no recurrence of oscillopsia during a follow-up of 22 months to date. From this single observation it appears likely that vascular compression of the trochlear nerve could be a significant pathophysiological factor contributing to SOM. In the hands of an experienced surgeon, microvascular decompression at the brainstem exit zone of this nerve may evolve as the method of choice for selected cases of disabling SOM.
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Journal of neurosurgery · Dec 1998
Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response.
Traumatic brain injury (TBI) is exacerbated by hypotension and hypoventilation. Because previous studies have shown a potentiating effect of ethanol (EtOH) on TBI and hemorrhagic shock (HS), the authors investigated the effects of EtOH on the early physiological response to TBI with and without HS. ⋯ In this model of TBI, acute EtOH intoxication in the presence of HS potentiates the physiological and metabolic alterations that may contribute to secondary brain injury.