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Query: UMLS:C0040822 (tremor)
18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report 7 cases of infants presenting with an apparent life-threatening event associated with acute pericerebral haemorrhage (subarachnoid haemorrhage and/or subdural hematoma) without evidence of traumatism, abuse, or shaking. Clinical characteristics were the same in all cases, including limpness, severe dysautonomic disorders, and pallor; all infants had retinal and pre-retinal haemorrhages. Two infants died; the five survivors have severe neurologic sequelae. The symptoms revealing an infant's pericerebral haemorrhage are usually axial hypotonia and pallor. Traumatism remains the most common aetiology and must be searched for. Non-traumatic aetiologies are unusual and were excluded in these reported cases. The 'shaken baby' syndrome is not the sole aetiology of an apparent spontaneous pericerebral haemorrhage: a slight bump associated with predisposing vascular factors particular to infancy could be involved. When confronted with an apparent life-threatening event associating limpness and pallor, one must consider the diagnosis of pericerebral haemorrhage.
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PMID:[Is pericerebral hemorrhage a cause of severe malaise in infants?]. 133 65

We examined the efficacy of slow-release, and prolonged diffusion silicone pellets mixed with papaverine hydrochloride in the treatment of cerebral vasospasms following subarachnoid hemorrhage. In addition the diffusion of the other vasodilating agents (diltiazem and nicardipine) into the saline solution using the same silicone materials was also investigated. Papaverine hydrochloride was either packed in silicone tubes (packed type) or polymerized with silicone elastomer, Silastic MDX-4-4210 (solid type). The solid type pellet is cylindrical-(diameter 3 mm, length 30 mm) and contains 40 w/v% of pure powder of papaverine. The amount of the delivered drug was measured for 5 weeks at 37 degrees C and at room temperature. The diffusion rate of the solid type pellet was about 5 times higher than that of the packed one. The diffusion rates of both types of pellets were about 10 times higher at 37 degrees C than at room temperature. The cummulative amount of the delivered drug from the solid type pellet was 37.1% of the initial packed volume at 37 degrees C in the first 3 weeks. The diffusion of diltiazem and nicardipine which were polymerized 30 w/v% in silicone elastomer was observed for 3 weeks at 37 degrees C only in solid type pellet form. The diffusion rate was measured under the condition of either continuous shaking or standing. The results showed the same diffusion rates for diltiazem and nicardipine, with no difference in diffusion rate between the "shaking" and "standing" groups. The diffusion rate showed inverse exponential curves, and was 5-20 X 10(-5)/day/mm2 of initial volume until 5 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sustained-release pellet of vasodilators--basic experiment]. 651 25

To prevent cerebral vasospasm after aneurysmal subarachnoid haemorrhage, cisternal irrigation has been reported to be more effective when combined with continuous head-shaking (head-shaking method). The present study was conducted to evaluate the safety and preventative effect for vasospasm in patients treated with the head-shaking method. Six of 17 patients managed postoperatively by the original head-shaking procedure developed neurological deterioration related to the method: two had intracranial haematoma (one with acute interhemispheric subdural haematoma, and the other with cerebellar haemorrhage), two had acute brain swelling, and two failed to show abnormal findings on computed tomography. These pathological processes may be suitably referred to as "head-shaking syndrome". Delayed ischaemic neurological deficits associated with low-density lesions on computed tomography were demonstrated in five patients (29%). From these observations, the head-shaking method may not be as safe as described in the original articles, and is critically evaluated in terms of its preventative effect for cerebral vasospasm.
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PMID:"Head-shaking syndrome" neurological deterioration during continuous head-shaking as an adjunct to cisternal irrigation for clot removal in patients with acute subarachnoid haemorrhage. 775 55

Vitreous hemorrhage is relatively common following subarachnoid hemorrhage, but rarely occurs after accidental head injury. In this paper, we report a rare case of vitreous hemorrhage after an accidental head injury with chest compression. A 4-month-old girl was held in her father's arms. After he fell down, she struck her head and her chest was compressed by her father's body. She soon became pale and was immediately transported to our center complaining of disturbance of consciousness on February 6, 1993. On admission, she was semicomatose and had a generalized convulsion. Computed tomography (CT) scan showed a subdural hematoma, although no fracture was detected on the plain X-ray film. Bilateral vitreous hemorrhage was also observed. The anterior fontanelle pressure was a high 330 mmH2O. The patient was treated conservatively with agents to promote hemostasis and reduce the intracranial hypertension. She was discharged after one month with normal consciousness and improved vision. The follow-up CT scan revealed subdural hematoma, hemorrhagic infarction (suggesting rupture of the pontine veins), and cerebral atrophy, corresponding to those of the shaken baby syndrome. Her chest was compressed by her father's body. The anterior fontanelle pressure was a high 330 mmH2O. These findings suggest that shaking or abrupt deceleration, acute intrathoracic hypertension and acute intracranial hypertension, caused retinal hemorrhage, and that extensive retinal hemorrhage possibly resulted in vitreous hemorrhage.
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PMID:[Vitreous hemorrhage after accidental head injury with chest compression--case report]. 787 84

A 25 year old man had an acute subarachnoid haemorrhage due to the rupture of a right peduncular subthalamic arteriovenous malformation. Seven months later he developed a left rest tremor associated with mild bilateral extrapyramidal symptoms and responsive to levodopa treatment. Surface EMG recording showed synchronous activity of agonist and antagonist muscles in the left limbs. A PET 18F-dopa study showed a large decrease of the Ki value in the right striatum. One year after the stroke a persistent postural component developed in the tremor.
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PMID:Rest tremor and extrapyramidal symptoms after midbrain haemorrhage: clinical and 18F-dopa PET evaluation. 805 26

The term "battered-child syndrome" was coined by Kempe in 1962. The morphology of brain lesions in abused children is rarely reported in Japan. This clinicopathological entity in the central nervous system is characterized by retinal hemorrhages, subdural and subarachnoid hemorrhage. However, reports on microscopic findings of intracerebral lesion are fewer than those on macroscopic findings of scalp, skull and intracranial cavity. This study was performed on 8 cases of battered children who were autopsied. They consisted of six female and two male infants. The age ranged from one week to four years old. The causes of the injuries were shaking in four cases, throwing in three cases, dropping in two cases and strangling in one case, mostly in combination. CT scans were examined for three cases. CT scan revealed acute cerebral swelling and acute subdural hematoma with interhemispheric blood clot in three cases and multiple low density area in one case. Evacuation of the subdural hematoma and external decompression was performed in one case. The survival period from injury to death was one day in four cases, and 2, 3, 9 and 41 days in the others. In the gross anatomical findings there are many excoriations and bruises of the face and scalp in five cases, widespread subcutaneous hematoma in all cases and skull fracture in only two cases. The brain weight was exceedingly heavier than normal brain weight by age in five cases. In the macroscopic findings, there were marked cerebral swelling and cerebral herniation in all cases, traumatic subarachnoid hemorrhage in six cases, and thin widespread acute subdural hematoma with interhemispheric clot in four cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuropathological study of battered child syndrome: eight autopsy cases]. 829 98

We hypothesize that apnea induced by shaking or by shaking combined with impact plays a major role in the pathophysiology of nonaccidental head trauma and accounts for the poor outcome in this subgroup of patients. In a retrospective study of 28 children who suffered significant nonaccidental head injury, 57% had a history of apnea prior to hospitalization, 82% were intubated upon admission, and 71% had early seizures. For further evidence of ischemia and hypoxia, the first recorded blood pressure was < 80 in 50% and the arterial pH < 7.3 in 54%. Seventy-one percent had diffuse brain swelling which is characteristic of cerebral hypoxia and/or ischemia on the first CT scan. None of the children who had clinical evidence of cerebral hypoxia or ischemia had a good outcome. We conclude that trauma-induced apnea causes cerebral hypoxia and/or ischemia which is more fundamental to outcome than the mechanism of injury (shaken vs. shaken with impact), subdural hemorrhage, subarachnoid hemorrhage, diffuse axonal injury, parenchymal shear, or brain contusion.
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PMID:Role of apnea in nonaccidental head injury. 874 99

One study has questioned the validity of shaking as a mechanism of head injury in children. A prospective, postmortem study investigated 80 deaths from head trauma to identify the roles of shaking and direct impacts. Evidence of shaking was defined as two or more of the following criteria: 1) finger marks and/or rib fractures, 2) subdural and/or subarachnoid hemorrhage, or 3) a history of vigorous shaking. Shaking to the exclusion of other head trauma was defined as the presence of two or more of the above criteria together with the complete absence of scalp or skull injuries. Nine (11.3%) of the 80 study deaths qualified as exclusively shaking injuries by this definition. Thirty (37.5%) of the deaths had direct injuries as well as two of the criteria of shaking; these deaths were classified as combined shaking and blunt trauma. Forty-one (51.3%) of the deaths had impact injuries without having two of the criteria of shaking. We reviewed the extent of ocular injuries in all the cases. We found ocular hemorrhages with increased frequency in cases with two or more of the criteria of shaking compared to cases with only impact mechanism of injury. Retinal hemorrhages continue to show themselves to be a good marker of infants injured by vigorous, intentional shaking. This study likewise confirms the observations of others that most, but not all, shaken babies have impact injuries as well.
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PMID:Shaken babies--some have no impact injuries. 878 36

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been
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PMID:[A 64-year-old woman with progressive gait disturbance and dementia for one year]. 978 11

This article represents the work of the National Association of Medical Examiners Ad Hoc Committee on shaken baby syndrome. Abusive head injuries include injuries caused by shaking as well as impact to the head, either by directly striking the head or by causing the head to strike another object or surface. Because of anatomic and developmental differences in the brain and skull of the young child, the mechanisms and types of injuries that affect the head differ from those that affect the older child or adult. The mechanism of injury produced by inflicted head injuries in these children is most often rotational movement of the brain within the cranial cavity. Rotational movement of the brain damages the nervous system by creating shearing forces, which cause diffuse axonal injury with disruption of axons and tearing of bridging veins, which causes subdural and subarachnoid hemorrhages, and is very commonly associated with retinal schisis and hemorrhages. Recognition of this mechanism of injury may be helpful in severe acute rotational brain injuries because it facilitates understanding of such clinical features as the decrease in the level of consciousness and respiratory distress seen in these injured children. The pathologic findings of subdural hemorrhage, subarachnoid hemorrhage, and retinal hemorrhages are offered as "markers" to assist in the recognition of the presence of shearing brain injury in young children.
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PMID:Position paper on fatal abusive head injuries in infants and young children. 1195 7


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