ABSTRACT
This case report describes the sporadic Creutzfeldt-Jakob disease (CJD) of a 53-year-old man who initially complained about vertigo and dizziness. Within 18 weeks, he developed impaired memory, hemineglect, and sensory impairment of the left half of the body. A CSF tap was positive for 14-3-3 protein and showed increased tau protein, neuron-specific enolase (NSE), and the astroglial protein S-100 B. The EEG showed right temporal sharp waves without periodicity. Diffusion-weighted MRI revealed hyperintensities in the right temporo-occipital cortex which corresponded well with hypometabolic areas in a PET scan and the neurological and neuropsychological deficits. The morphological FLAIR T2 MRI showed no pathological changes. Within 20 weeks, the patient developed severe dementia with decreased spatial orientation and myoclonia, became incontinent, and was confined to bed. He died within 22 weeks after the first presentation of symptoms.
Subject(s)
Creutzfeldt-Jakob Syndrome/diagnosis , Dementia/diagnosis , Diffusion Magnetic Resonance Imaging/methods , Hemiplegia/diagnosis , Neurologic Examination , Perceptual Disorders/diagnosis , Diagnosis, Differential , Electroencephalography , Fatal Outcome , Follow-Up Studies , Humans , Male , Middle Aged , Neuropsychological Tests , Occipital Lobe/pathology , Temporal Lobe/pathology , Tomography, Emission-Computed , Vertigo/etiologyABSTRACT
An increased daily alcohol consumption results in neurological symptoms and morphological central nervous system changes, e.g. shrinkage of the frontal lobes and the cerebellar vermis. Brain shrinkage can be due to neuronal loss, gliosis, or alterations of (cell) membrane constitutes/myelin. Neuronal, glial, and metabolic changes can be measured in vivo with proton magnetic resonance spectroscopy. A total of 11 alcoholics and 10 age-matched volunteers were examined by magnetic resonance imaging and localized magnetic resonance spectroscopy at an echo time of 135 and 5 msec. Peak integral values were calculated for N-acetylaspartate (NAA), choline (Cho), myo-inositol (ml), glutamate/glutamine (Glx), and normalized to phosphocreatine/creatine (Cr). Patients had a significant shrinkage of the cerebellar vermis. NAA/Cr and Cho/Cr ratios were reduced in both sequences, but the NAA/Cr reduction was only significant in long echo time, although the Cho/Cr reduction was significant in short echo time. The ml/Cr and Glx/Cr ratios did not show any significant difference between volunteers and patients. The decrease of NAA/Cr in alcohol dependent patients is consistent with neuronal loss. The Cho/Cr decrease and an unchanged ml/Cr may reflect cell membrane modification or myelin alterations in alcohol-dependent patients. These changes lead to brain shrinkage, although hydration effects and gliosis are less likely.
Subject(s)
Alcoholism/pathology , Cerebellum/pathology , Magnetic Resonance Imaging , Adult , Aged , Alcoholism/metabolism , Aspartic Acid/analogs & derivatives , Aspartic Acid/metabolism , Atrophy/pathology , Cerebellum/metabolism , Choline/metabolism , Female , Humans , Male , Middle AgedABSTRACT
Although treatment outcome in alcoholism is good and well documented, many patients are not sufficiently motivated for participating in a treatment program. The following case-report illustrates the example of a young male alcoholic suffering from decompensated liver cirrhoses without motivation for a long-term treatment. The positive effects of the new guidelines of the laws regulating custody and civil commitment are shown and discussed.
Subject(s)
Alcoholism/rehabilitation , Commitment of Mentally Ill/legislation & jurisprudence , Legal Guardians , Liver Cirrhosis, Alcoholic/rehabilitation , Adult , Germany , Humans , Male , MotivationABSTRACT
The authors deal with the heuristic value of the "neurobiological model of alcohol dependence". It allows the study of the influence of a defined noxe on different brain structures. Additionally, it enables the quantification of regeneration and restitution processes in abstinence. Because of this, the alcoholism model goes beyond dementia, the model which has dominated brain research so far. Neuropathological studies in humans and animals found a reduction in the volume of white matter and a partial degeneration, or even loss of specific neurons. According to animal data, this could to a certain extent be genetically determined. Alcohol exerts a distinct influence on different neurotransmitter systems. This research will deepen our understanding of the neurotoxic and psychotropic properties of alcohol, and of the development of dependence. Little is known about the role of astrocytes in the reaction of the brain to alcohol. Here again, the neurobiological model of alcohol dependence could be of value in learning more about their interactions with neurons. Using Magnetic Resonance Imaging and CAT-scans, the decrease in volume of white and grey matter was demonstrated in vivo. The degree and the time course of brain damage seems to be influenced less by drinking history than by age and gender. There is evidence that female alcoholics develop brain damage more readily than men. When abstinent, an increase in the volume of white and grey matter can be observed. This is not due to the rehydration of brain tissue alone. Future research will need to deal with the question of whether the central nervous system is capable of partial regeneration. For the study of neuroplasticity, the neurobiological model of alcohol dependence seems to be particularly well suited.
