Cerebral atrophy

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

VS blood pressure 128/62 mm Hg supine, pulse 77 beats per minute, respiratory rate 15/minutes, temperature 37°C (98.6°F) Gen Poorly-groomed, thin woman looks stated age Neuro Folstein Mini Mental Status Exam score 16/30 disoriented to month, date, and day of week, clinic name and floor poor registration with impaired attention and shortterm memory recalled 0 out of 3 items good language skills but problems with commands CT Scan Mild to moderate generalized cerebral atrophy... 

Co BT, Goodwin DW, Gado M, Mikhael M and Hill SY (1977). Absence of cerebral atrophy in chronic cannabis users. Journal of the American Medical Association, 237, 1229-1230. 

Phosphoenolpyruvate carboxykinase (PEPCK) deficiency is distinctly rare and even more devastating clinically than deficiencies of glucose-6-phosphatase or fructose-1,6-bisphosphatase. PEPCK activity is almost equally distributed between a cytosolic form and a mitochondrial form. These two forms have similar molecular weights but differ by their kinetic and immunochemical properties. The cytosolic activity is responsive to fasting and various hormonal stimuli. Hypoglycemia is severe and intractable in the absence of PEPCK [12]. A young child with cytosolic PEPCK deficiency had severe cerebral atrophy, optic atrophy and fatty infiltration of liver and kidney. 

Defects of the Krebs cycle. Fumarase deficiency was reported in children with mitochondrial encephalomyop-athy. Usually, there is developmental delay since early infancy, microcephaly, hypotonia and cerebral atrophy, with death in infancy or early childhood. The laboratory hallmark of the disease is the excretion of large amounts of fumaric acid and, to a lesser extent, succinic acid in the urine. The enzyme defect has been found in muscle, liver and cultured skin fibroblasts [16]. 

Bowden CL, Brugger AM, Swann AC, et al Efficacy of divalproex vs lithium and placebo in the treatment of mania. JAMA 271 918-924, 1994b Bowen DM, Davison AN Biochemical studies of nerve cells and energy metabolism in Alzheimer s disease. Br Med Bull 42 75-80, 1986 Bowen DM, Smith CB, White P Accelerated ageing or selective neuronal loss as an important cause of dementia Lancet 1 11-14, 1979 Bowen DM, Smith CB, White P, et al Biochemical assessment of serotonergic and cholinergic dysfunction and cerebral atrophy in Alzheimer s disease. J Neuro-chem 41 266-272, 1983... 

The clinical significance of these CT scan alterations is unknown, and it is important to note that two similar studies found no statistically significant differences between the CT scans of long-term BZD users and matched control subjects ( 212, 213). Poser et al. (212) did find, however, that patients with combined BZD—alcohol dependence showed some degree of cerebral atrophy. Uhde and Kellner (211) also observed that the apparent association between VBR and duration of BZD exposure may be secondary to alcohol consumption, because long-term BZD users also may be more frequent users, but not necessarily abusers, of alcohol. 

Poser W, Poser S, Roscher D, et al. Do benzodiazepines cause cerebral atrophy [Letter], Lancet 1983 1 715. 

There is a higher frequency of cognitive Impairment, cerebral atrophy, white matter changes. 

Long-term treatment with glucocorticoids can cause cerebral atrophy (44). 

Bentson J, Reza M, Winter J, Wilson G. Steroids and apparent cerebral atrophy on computed tomography 63. scans. J Comput Assist Tomogr 1978 2(l) 16-23. 

Generally, but not invariably, postmortem macroscopic examination of the brain reveals cerebral atrophy with narrowed convolutions, widened sulci, and enlarged lateral and third ventricles. On microscopic examination brain specimens from patients with a clinical diagnosis of Alzheimer s disease are characterized by widely spread cortical senile plaques, neurofibrillary tangles, and granulovascular degeneration. 

A CT scan or MRI of the brain following a strokelike episode reveals a lucency (an area of luminosity) that is consistent with infarction. Later, cerebral atrophy and calcifications may be observed on brain imaging studies. The vascular territories of focal brain lesions and the prior medical history of these patients differ substantially from those of typical patients with stroke. Serial MRI studies often demonstrate lesion resolution, differentiating these lesions from typical ischemic strokes. An electroencephalogram is often performed when seizures are a concern. This is especially necessary in MELAS since patients occasionally have intractable status epilepticus as a terminal condition. Mental deterioration usually progresses after repeated episodic attacks. Psychiatric abnormalities (e.g., altered mental status, schizophrenia) may accompany the strokelike episodes. The encephalopathy may progress to... 

Jellinck, E. H. (1976). Cerebral atrophy and cognitive impairment in chronic schizophrenia. The Lancet, 2, 1202-1203. 

Although the nature of the brain abnormalities seen in schizophrenia is not clearly known at present, certain pieces of the puzzle are being identified. Overall, schizophrenic patients appear to have some degree of cerebral atrophy (about 5% loss of cerebral mass), enlarged cerebral ventricles, and decreased size of certain other brain structures. From a functional perspective, the prefrontal and medial temporal brain appear to be particularly affected. Several neurochemical abnormalities are also associated with the disorder, and several neurotransmitter systems have been implicated (Table 5.5). 

However, neuropathological examination in three patients with temporal lobe atrophy and vascular dementia found no evidence of Alzheimer s type pathology in the cortex (Fein et al. 2000). Therefore, medial temporal lobe atrophy is not specific to Alzheimer s dementia. However, it maybe of some discriminatory value in early disease (Jobst et al. 1998 O Brien et al. 2000), although this may be less so in elderly patients in whom medial temporal lobe atrophy may simply reflect age-related cerebral atrophy. 

Brickman AM, Honig LS, Scarmeas N, Tatarina O, Sanders L, Albert MS, Brandt J, Blacker D, Stem Y (2008) Measuring cerebral atrophy and white matter hyperintensity burden to predict the rate of cognitive decline in Alzheimer disease. Arch Neurol 65(9) 1202-1208 Brody DL, Magnoni S, Schwetye KE, Spinner ML, Esparza TJ, Stocchetti N, Zipfel GJ, Holtzman DM (2008) Amyloid-beta dynamics correlate with neurological status in the injured human brain. Science 321(5893) 1221-1224... 

An 82-year-old man with left ventricular dysfunction and gout had worsening renal function (33). He was taking lisinopril, furosemide, naproxen, allopurinol, and baclofen 20 mg tds. As no reason could be found for the use of baclofen the dose was halved and then stopped 10 days later. The next day he had visual hallucinations, confusion, and agitation, and required sedation with diazepam. He was afebrile, with normal inflammatory markers, and a CT scan of the brain showed only cerebral atrophy. Baclofen was reintroduced, with complete resolution of neuropsychiatric symptoms within 48 hours. 

Toxicity associated with chronic use is not as well described as acute toxicity, but it appears to include cerebral atrophy, cardiomyopathy, and chronic pulmonary disease. Cocaine and its metabolites are most commonly identified in patient urine. An immunoassay directed toward identification of benzoyl-ecgonine will frequently indicate the presence of cocaine and its metabolites for many days after use. The duration of qualitatively detected cocaine and metabolites in urine is probably dose dependent and may be up to 3 weeks in length. Chronic use of cocaine may lead to dependence. 

Chronic effects associated with occupational exposures to turpentine include cerebral atrophy, behavioral changes, anemia, bone marrow damage, glomerulonephritis, and dermatitis. Urinary disturbances, albuminuria, and urinary casts were observed in workers exposed to paints and varnishes. Elowever, renal damage associated with occupational exposures to turpentine was transient and reversible. 

There are also very rare recessive inherited diseases that result from defects in the biosynthesis of molybdenum cofactor in most cases they result in early childhood death, hirst symptoms are failure to thrive and seizures in later stages lens dislocations are noted together with cerebral atrophy. Disease-causing mutations have been located, and the possibility of gene therapy is being investigated." ... 

This condition has been described by Rett (RIO, Rll) and Rett and Stockl (R12) in 22 children, all girls, the oldest of them 13 years of age, from a survey of 6000 mentally subnormal children. In all 22, the blood ammonia was raised from 2 to 5 times the normal the highest being 165 /ig/100 ml. The blood urea was said to be normal in all cases, as was the plasma amino acids. Where liver biopsy was obtained, this was also normal. The brain was examined in 5 children who died. They showed cerebral atrophy but no Alzheimer Type II cells. A relationship between hyperammonemia and the cerebral changes of the syndrome was postulated and attention drawn to the similarity with some of the neurological manifestations of children with urea cycle defects. However, the cause of the hyperammonemia was unexplained, and it seems unlikely that these were examples of primary urea cycle disorders. 

Hereditary sulfite oxidase deficiency can occur alone or with xanthine oxidase deficiency. Both enzymes contain molybdenum (Chapter 27). Patients with sulfite oxidase deficiency exhibit mental retardation, major motor seizures, cerebral atrophy, and lens dislocation. Dietary deficiency of molybdenum (Chapter 37) can cause deficient activity of sulfite and xanthine oxidases. 

Campbell AM, Evans M, Thomson JL, Williams MJ (1971) Cerebral atrophy in young cannabis smokers. Lancet 2 1219-1224... 

Archer HA, Edison P, Brooks DJ, Barnes J, Frost C, Yeatman T (2006) Amyloid load and cerebral atrophy in Alzheimer s disease all C-BIP positron emission tomography study. Ann Neurol 60 145-147... 

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