Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Case report.

Hypertrophic olivary degeneration (HOD) is a rare type of neuronal degeneration involving the dento-rubro-olivary pathway and presents clinically as palatal tremor. We present a 48 year old male patient who developed Holmes' tremor and bilateral HOD five months after brainstem hemorrhage. The severe rest tremor was refractory to pharmacotherapy and botulinum toxin injections, but was markedly reduced after thalamotomy. Magnetic resonance imaging permitted visualization of HOD, which appeared as a characteristic high signal intensity in the inferior olivary nuclei on T2- and proton-density-weighted images. Enlargement of the inferior olivary nuclei was also noted. Palatal tremor was absent in that moment and appears about two months later. The delayed-onset between insult and tremor following structural lesions of the brain suggest that compensatory or secondary changes in nervous system function must contribute to tremor genesis. The literature and imaging findings of this uncommon condition are reviewed.

Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Case report

Hypertrophic olivary degeneration (HOD) is a rare type of neuronal degeneration involving the dento-rubro-olivary pathway and presents clinically as palatal tremor. We present a 48 year old male patient who developed Holmes' tremor and bilateral HOD five months after brainstem hemorrhage. The severe rest tremor was refractory to pharmacotherapy and botulinum toxin injections, but was markedly reduced after thalamotomy. Magnetic resonance imaging permitted visualization of HOD, which appeared as a characteristic high signal intensity in the inferior olivary nuclei on T2- and proton-density-weighted images. Enlargement of the inferior olivary nuclei was also noted. Palatal tremor was absent in that moment and appears about two months later. The delayed-onset between insult and tremor following structural lesions of the brain suggest that compensatory or secondary changes in nervous system function must contribute to tremor genesis. The literature and imaging findings of this uncommon condition are reviewed

Cerebral trypanosomiasis and AIDS.

UNLABELLED: A 36 year-old black female, complaining of headache of one month's duration presented with nausea, vomiting, somnolence, short memory problems, loss of weight, and no fever history. Smoker, intravenous drugs abuser, promiscuous lifestyle. PHYSICAL EXAMINATION: left homonimous hemianopsia, left hemiparesis, no papilledema, diffuse hyperreflexia, slowness of movements. Brain CT scan: tumor-like lesion in the splenium of the corpus calosum, measuring 3.5 x 1.4 cm, with heterogeneous enhancing pattern, suggesting a primary CNS tumor. Due to the possibility of CNS infection, a lumbar puncture disclosed an opening pressure of 380 mmH(2)0; 11 white cells (lymphocytes); glucose 18 mg/dl (serum glucose 73 mg/dl); proteins 139 mg/dl; presence of Trypanosoma parasites. Serum Elisa-HIV tests turned out to be positive. Treatment with benznidazole dramatically improved clinical and radiographic picture, but the patient died 6 weeks later because of respiratory failure. T. cruzi infection of the CNS is a rare disease, but we have an increasing number of cases in HIV immunocompromised patients. Diagnosis by direct observation of CSF is uncommon, and most of the cases are diagnosed by pathological examination. It is a highly lethal disease, even when properly diagnosed and treated. This article intends to include cerebral trypanosomiasis in the differential diagnosis of intracranial space-occupying lesions, especially in immunocompromised patients from endemic regions.

Cerebral trypanosomiasis and AIDS

A 36 year-old black female, complaining of headache of one month's duration presented with nausea, vomiting, somnolence, short memory problems, loss of weight, and no fever history. Smoker, intravenous drugs abuser, promiscuous lifestyle. Physical examination: left homonimous hemianopsia, left hemiparesis, no papilledema, diffuse hyperreflexia, slowness of movements. Brain CT scan: tumor-like lesion in the splenium of the corpus calosum, measuring 3.5 x 1.4 cm, with heterogeneous enhancing pattern, sugesting a primary CNS tumor. Due to the possibility of CNS infection, a lumbar puncture disclosed an opening pressure of 380 mmH(2)0; 11 white cells (lymphocytes); glucose 18 mg/dl (serum glucose 73 mg/dl); proteins 139 mg/dl; presence of Trypanosoma parasites. Serum Elisa-HIV tests turned out to be positive. Treatment with benznidazole dramatically improved clinical and radiographic picture, but the patient died 6 weeks later because of respiratory failure. T. cruzi infection of the CNS is a rare disease, but we have an increasing number of cases in HIV immunecompromised patients. Diagnosis by direct observation of CSF is uncommon, and most of the cases are diagnosed by pathological examination. It is a highly lethal disease, even when properly diagnosed and treated. This article intends to include cerebral trypanosomiasis in the differential diagnosis of intracranial space-occupying lesions, especially in immunecompromised patients from endemic regions