[A patient with Creutzfeldt-Jakob disease supported by home medical care from the stage of disease progression to death through hospital-clinic cooperation and medical-welfare cooperation].

The patient was a 63-year-old woman who presented with slowness of speech after cerebral infarction. Diffusion-weighted MR images and investigations of cerebrospinal fluid showed abnormal values, and the patient was diagnosed as having sporadic Creutzfeldt-Jakob disease(CJD). This is an intractable disease and affects one in one million people; it progresses relatively rapidly, eventually resulting in death. For procedures such as intravenous fluid replacement and the treatment of pressure sores, we require thorough hand washing, eye protection, and disposal of gloves and dressings by incineration. It is desirable for patients to spend the limited amount of time available to them peacefully at home with their family. Visiting physicians and nurses need to take the initiative in sharing information obtained from the CJD infection control guidelines and core hospitals with welfare personnel such as caregivers, in order to provide correct information on all aspects of patient care and the management of this disease in the home environment. Excellent supportive care was provided for the patient at home, and she passed away with her family by her side.

Acute encephalomyelitis associated with acute viral hepatitis type B.

We describe the case of a 36-year-old woman who developed acute encephalo-myelitis after acute viral hepatitis type B. She was admitted to the hospital with a history of general malaise and nausea of 5 days duration. Her serum showed high transaminase levels and positive HBs-Ag and increased IgM HBc-Ab titers. She had urinary dysfunction, myoclonus and postural tremor of her extremities. Several days later, she developed bilateral limb ataxia and alteration of consciousness. The cerebrospinal fluid examinations showed pleocytosis and increased protein. Treatment with high-dose methylprednisolone resulted in a marked improvement of the clinical and CSF examination. Magnetic resonance imaging of the brain and the spinal cord did not disclose abnormal lesions. The symptoms and clinical course were quite similar to those of acute disseminated encephalomyelitis.

A compensatory mechanism in unilateral akinetic-rigid syndrome: an fMRI study.

The motor mechanisms of a patient with unilateral hand clumsiness in the early stages of akinetic-rigid syndrome were assessed by functional magnetic resonance imaging (fMRI). Movements of the unaffected hand produced activation in the contralateral sensorimotor cortex (SMC) and ipsilateral SMC and superior parietal lobule (SPL). The affected hand activated the bilateral SMCs, supplementary motor areas, and SPLs. We speculated that the bilateral activation indicated recruitment of a pre-existing bilaterally organized large-scale neural network to perform the motor task.

The mechanisms of recovery from cerebellar infarction: an fMRI study.

Patients with cerebellar infarction frequently make an excellent functional recovery. However, the mechanisms of functional recovery from cerebellar infarction remain unclear. Thus, functional MRI was used to investigate these mechanisms in six right-handed patients with complete recovery after cerebellar infarction, and nine right-handed normal subjects. The non-infarcted side of the cerebellum and the sensorimotor cortex contralateral to the non-infarcted side of the cerebellum were significantly activated during the infarcted-side hand movement. In the infarcted side of the cerebellum, intact regions were activated. Our results indicate that recovery from cerebellar infarction depends on reorganization in the infarcted side of the cerebellum, and recruitment of the cerebellocortical loop involving the cerebrum ipsilateral to the movement and the cerebellum contralateral to the movement.