Cases reported "Cerebral Palsy"

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1/5. A patient with cerebral palsy whose mother had a traffic accident during pregnancy: a diffuse axonal injury?

    A 16-year-old girl had spastic cerebral palsy (CP) with triplegia and focal epilepsy. The patient's past history included her mother's lower abdominal trauma caused by a traffic accident at the 7th month of gestation. Brain examination with magnetic resonance imaging (MRI) revealed encephalomalacia at the bilateral parieto-temporal lobes and the left caudate nucleus, segmental narrowing of the splenium of the corpus callosum, dilatation of the left lateral ventricle and an abnormally high intensity at the right posterior portion of the internal capsule. These findings might indicate a diffuse axonal injury (DAI), but not an asphyxic brain damage. In this patient, CP might be caused by an intrauterine DAI when her mother was involved in the accident.
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2/5. Chronic self-stimulation of the dentate nucleus for the relief of spasticity.

    It has been assumed but not yet proved that cerebellar cortical stimulation activates the purkinje cells, with subsequent inhibition of the deep cerebellar nuclei. However, the relatively crude, widespread excitation induced by several surface electrode arrays and the parameters of stimulation currently used, may produce other effects than selective activation of only one specific cellular type which, furthermore, seems to be rarely present in these particular patients, as demonstrated by biopsy studies prior to electrode placement. The dentate nucleus was chronically implanted with a stimulating system in a patient with spasticity due to cerebral palsy. Chronic self-stimulation induced a significant improvement in motor function, with relief of spasticity and improvement in speech, posture, balance and gait. Electrophysiological studies demonstrated a decrease in the amplitude of V1 and V2 responses and in the H/M and T/M ratios, an increase in the silent period, and marked effects in the H reflex recovery curve, as well as diminished contralateral cortical somato-sensory evoked potentials. This result seems to indicate that the clinical effects of cerebellar cortical stimulation are not due to prosthetically induced inhibition of the dentate nucleus.
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3/5. Vertical gaze palsies from medial thalamic infarctions without midbrain involvement.

    BACKGROUND: Although the supranuclear pathways for vertical gaze control are not well defined, lesions of the mesencephalic reticular formation including the nucleus of Darkschewitsch, the rostral interstitial medial longitudinal fasciculus, the interstitial nucleus of Cajal, and the posterior commissure are known to produce vertical gaze palsies. MRI studies have not previously reported isolated thalamic lesions as the cause of vertical gaze palsies. CASE DESCRIPTIONS: Three patients with acute paralysis of vertical gaze were imaged with MRI. Sagittal T1 and axial T1, T2, and proton-weighted images were obtained. All three patients had repeated scans performed from 3 days to 6 weeks after the original study. Two patients exhibited unilateral right thalamic infarcts (polar and paramedial territory), and one patient had a bilateral paramedian thalamic infarction. There was no evidence of midbrain involvement on any of the images. CONCLUSIONS: Vertical gaze palsies are known to be produced by lesions of the rostral interstitial medial longitudinal fasciculus. This MRI study reveals thalamic infarctions without associated midbrain infarctions in three patients with vertical gaze palsies. This may be explained by interruption of supranuclear inputs.
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keywords = nucleus
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4/5. Two cases of maternal antenatal splenic rupture and hypotension associated with Moebius syndrome and cerebral palsy in offspring. Further evidence for a utero placental vascular aetiology for the Moebius syndrome and some cases of cerebral palsy.

    We wish to report two cases of congenital abnormality after antenatal car accidents resulting in ruptured spleen and severe hypotension in the mothers at 8 and 14 weeks gestation. The first case had the classical Moebius syndrome with 6th and 7th cranial nerve palsy with abnormal brain stem evoked responses, presumably due to hypoxic/ischaemic brain stem damage and the second case had severe retardation and hypertonic cerebral palsy which at post mortem was found to be due to old hypoxic/ischaemic lesions to the caudate nucleus putamen and striatum. Conclusion: The cases described provide evidence that severe maternal hypotension during pregnancy can be associated with lesions to the midbrain and brain stem of offspring. The mechanism is probably utero-placental insufficiency, and extrapolation from these two unusual cases would support utero-placental insufficiency as a cause of Moebius syndrome and limb deficiency after chorionic villus sampling.
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5/5. Rolandic type cerebral palsy in children as a pattern of hypoxic-ischemic injury in the full-term neonate.

    Magnetic resonance images (MRIs) of the brains of 11 patients aged from 1 week to 12 years with a distinctive type of cerebral palsy were selected based on distribution of cerebral lesions, which were restricted to bilateral perirolandic cortical and subcortical regions, including frequent symmetric involvement of basal ganglia and ventrolateral nucleus of thalami. Retrospectively, the perinatal history and clinical features were reviewed to correlate clinical data with this distinctive pattern of brain injury. Clinically affected neonates had an encephalopathy associated with a severe perinatal asphyxial event. Older children with cerebral palsy survived a similar perinatal course and demonstrated spastic quadriparesis with bulbar or pseudobulbar involvement, lack of verbal speech and variable delays in cognitive development. The distribution of hypoxic-ischemic lesions involving bilateral perirolandic regions, basal ganglia, and thalami, appears to correlate with increased metabolic areas of primary myelination in full-term neonates, but not with arterial border zones nor a single cerebral artery distribution. Myelination is a critical process in maturing brain associated with marked increase in tissue respiration and thus greater susceptibility to oxygen deprivation. It is believed that the extent of hypoxic-ischemic brain injury is determined principally by brain maturity and regional metabolic rates at time of insult and this correlates with active myelination in full-term neonates. This study confirms previous data from neuropathologic literature and recent reports of neuroimaging studies of asphyxiated neonates. In addition, retrospective analysis of the clinical data enables recognition of a type of cerebral palsy that might be the hallmark of hypoxic-ischemic injury in term neonates.
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