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Introduction. Using electroencephalography (EEG) and histology in patients with diffuse encephalopathy, Gloor et al reported that paroxysmal synchronous discharges (PSDs) on EEG required combined cortical gray (CG) and “subcortical” gray (SCG) matter pathology, while polymorphic delta activity (PDA) occurred in patients with white matter pathology. In patients with encephalopathy, we compared EEG findings and magnetic resonance imaging (MRI) to determine if MRI reflected similar pathological EEG correlations. Methods. Retrospective case control study of 52 cases with EEG evidence of encephalopathy and 50 controls without evidence of encephalopathy. Review of clinical, EEG and MRI data acquired within 4 days of each other. Results. The most common EEG finding in encephalopathy was background slowing, in 96.1%. We found PSDs in 0% of cases with the combination of CG and SCG abnormalities. Although 13.5% (n = 7) had PSDs on EEG; 3 of these had CG and 4 had SCG abnormalities. A total of 73.1% (38/52) had white matter abnormalities—of these 28.9% (11/38) had PDA. Conclusion. PSDs were found with either CG or “SCG” MRI abnormalities and did not require a combination of the two. In agreement with Gloor et al, PDA occurred with white matter MRI abnormalities in the absence of gray matter abnormalities.

Cerebral malaria (CM) is the most severe neurological presentation of acute falciparum malaria. It is a medical emergency, the hallmark of which is the presence of coma probably due to diffuse encephalopathy. A compromised microcirculation with sequestration of parasitized erythrocytes is central to the pathogenesis of cerebral malaria. The death is unacceptably high even with effective antimalarials in tertiary care hospital. The mainstay of treatment of cerebral malaria include prompt diagnosis and early institution of effective antimalarial therapy, recognition of complications, and appropriate supportive management in an ICU. Neurological sequlae are increasingly recognized, but further research on the pathogenesis of coma and neurological damage is required to develop other ancillary treatmentsNorthern International Medical College Journal Vol.6(2) 2015: 45-47

Cerebrovascular complications are one of the primary sources of morbidity and disability following cardiac surgery (1-3). Rapid improvements in myocardial preservation and continuing refinements in surgical technique have markedly reduced postoperative cardiovascular morbidity and mortality. As a result, surgery is offered to an increasing proportion of elderly patients, resulting in an increased incidence of postoperative cerebrovascular complications (4). Because more than 250,000 cardiac surgical procedures are performed each year, as many as 10,000 frank strokes and at least 50-100,000 less severe, but clinically evident, neurologic, neuropsychologic, and neuro-ophthalmologic deficits result from these procedures. The significant incidence of postoperative neurologic deficits is recorded in the literature (Table 1). If subtle cognitive deficits and biochemical evidence of neuronal injury are included, the incidence of cerebrovascular sequelae exceeds 75%. Following valvular surgery, the incidence of major cerebrovascular complications is even greater. Although some of these deficits resolve with time, others persist as sources of substantial disability for otherwise functional patients. We intend to measure different types of neurologic deficit. The variables include: the type of surgery, the age of the patient, whether the study is done on a prospective or retrospective basis, how and when are the patients examined, how sensitive is the testing, such as the neuropsychologic testing, and then one always has to consider the preconceived bias of the investigators. Ifwe are looking at neurologic outcome after bypass surgery, what should we look at? Frank stroke, whether there is presence or absence of acute or sustained diffuse encephalopathy, more subtle neuro

Severe epilepsy with multiple independent spike foci is an electroclinical entity with the following characteristics: (1) EEG showing multiple independent spike foci (three or more foci in both hemisphere, i.e., at least one in each hemisphere) and diffuse slowing of the background activity, (2) very frequent multiple types of seizures but mainly generalized minor seizures, (3) frequent association with mental retardation and neurologic abnormalities, (4) underlying causes of various nonspecific prenatal, perinatal, and postnatal cerebral conditions, and (5) poor prognoses for seizures and psychomotor development. It represents a diffuse encephalopathy with mutual transition between other age-dependent epileptic encephalopathies. This electroclinical condition may be appropriately named Markand-Blume-Ohtahara syndrome, after Markand and Blume, who initially described in detail the EEG pattern of multifocal spike discharges with its major clinical correlates, and Ohtahara, who extensively studied the group of patients with both clinical and EEG characteristics and proposed the concept of severe epilepsy with multiple independent spike foci, classifying it as one type of generalized epilepsy.

This peculiar 11-14 Hz spindle activity appears predominantly in the frontal area, and was observed in eight patients with impaired consciousness caused by nontraumatic diffuse encephalopathy. Characteristic of this frontal spindle activity is its transience and accordance with changes in the arousal level of the patient. When the degree of impaired consciousness in the patient was minimal and clinically not very apparent, this spindle activity appeared during light drowsiness. In lethargic patients, it was observed when the patient's level of consciousness rose (e.g. immediately after opening and closing the eyes). These frontal spindles disappeared at the onset of Stage 2 sleep, when normal physiologic spindle waves that are dominant in the vertex area appeared. A paroxysmal discharge was sometimes recorded in association with the frontal spindle activity and it disappeared at about the same time as these spindles. The prognosis was satisfactory for all patients in whom frontal spindle activity was observed; its correlation to spindle coma is also studied.

This case presents multiple and complex ethical as well as medical issues. The first issue to be resolved is medical; i.e., is this a dying patient or a chronically ill patient? From the details given, the question of the permanence of her brain damage cannot be resolved. Three and a half months is too short a time to answer the question clinically. The EEG findings were nonspecific, and the CT scans were normal. None of the medical complications listed were necessarily terminal. Therefore, this is a chronically ill patient with a diffuse encephalopathy of unknown etiology and is not a dying patient. This distinction is crucial. It is certainly acceptable to withhold useless or irrelevant treatment in the face of a progressive terminal disease. It is probably also permissible to refrain from treating complicating disease processes in a chronically ill patient when the chance of success is very poor. That was not the case with this patient.

Acquired immune deficiency syndrome (AIDS) has become a major public health problem with over 12,000 cases and 6,000 deaths reported to date. Although there has been an explosion of knowledge in the virology, immunology and pathology of AIDS, relatively little has been written on the neuropsychiatric aspects. This report reviews the existing literature on the neuropsychiatric complications of AIDS. As many as 40 percent of patients with AIDS have neurologic complications at some point in their illness. These complications include either focal deficits attributable to opportunistic organisms infecting the CNS or diffuse encephalopathy caused by viral infection or lymphoma infiltration. Psychiatric complications include major depression, adjustment disorder with depressed mood, and organic brain syndrome with affective, delusional or demented features. Inpatient and consulting psychiatrists must be alert to these complications of AIDS so as to make accurate diagnoses and deliver appropriate therapy. Further studies, integrating both psychiatric and neurologic perspectives, are needed to better elucidate the neuropsychiatric complications of AIDS and help plan appropriate therapeutic interventions.

From a group of 66 patients with the Lennox-Gastaut syndrome, 12 whose manifestations had started after the 6th year of life were selected for study. These patients were observed clinically and electroencephalographically for an average period of 2.5 years. We concluded that the late-onset syndrome can: occur after a long interval between diffuse encephalopathy and the first clinical manifestations, with or without previous alterations in psychomotor development; be associated from the onset with serious mental retardation; exhibit simple, complex and mixed seizures similar to those observed in the early form. These patients can also: suffer complex and mixed epileptic seizures previously unreported; paroxismal interictal EEG abnormalities that overlap those of the early form; and spike-slow wave complexes in the EEG that can be actived by hyperpnea. Our results demonstrate that the incidence of LGS after 6 years of age does not necessarily imply a lower frequency of organic antecedents, or beter neu-ropsychomotor development up to the onset of the syndrome or the presence of a higher rate of nonspecific seizures (generalized or partial seizures, and mainly those with elaborate symptomatolgy). The critical and encephalographic expression of the syndrome, which is secondary and starts after the 6th year of age, may depend at least in part on the age when diffuse encephalopathy started. De um grupo de 66 pacientes com sindrome de Lennox-Gastaut (SLG), selecionaram-se e se observaram 12 com manifestações sindrômicas se iniciando após o 6º ano de vida. Esses pacientes foram observados clínica e eletrencefalograficamente durante um período médio de 2,5 anos. Concluiu-se que a sindrome com início tardio pode: ocorrer após um longo intervalo entre a agressão encefálica difusa e as primeiras manifestações clínicas com ou sem alteração prévia do desenvolvimento psicomotor; associar-se, desde o início, a retardo mental grave; apresentar semiologia crítica (simples, complexa ou mista) semelhante à da forma precoce. Esses pacientes podem ainda apresentar: crises epilépticas complexas e mistas não referidas anteriormente na literatura; anormalidades EEG paroxísticas intercríticas que se sobrepõem às da forma precoce; no EEG complexos ponta-onda lenta que podem ser ativados pela hiperpnéia. Nossos resultados demonstram que a incidência da SLG após os 6 anos de idade, necessariamente não implica em menor freqüência de antecedentes orgânicos, em melhor desenvolvimento neuropsicomotor até o início da síndrome e na presença de maior proporção de crises não específicas (generalizadas ou parciais, principalmente as com sintomatologia elaborada). A expressão crítica e eletrencefalográfica da síndrome, secundária e se iniciando após o 6º ano de vida, poderia, pelo menos em parte, ser dependente da idade em que incidiu a agressão encefálica difusa.

Forty-two patients who had bursts of spontaneous, bilaterally synchronous slow waves during the waking state in an otherwise normal EEG were compared with 42 age-matched control subjects with normal EEGs. The study group had a significantly higher incidence of diffuse encephalopathy than did the control group. They also had a higher incidence of alterations of consciousness. None of the patients in the study group had focal, deep midline lesions. This study indicates that generalized, bilaterally synchronous slow bursts in the EEG are significant abnormalities that in the majority of cases are associated with a mild to moderate diffuse encephalopathy rather than with a lesion limited to deep midline structures.

Summary The case of a man who developed an acute encephalopathy at the end of a six weeks' course of streptomycin is described: he recovered slowly over two months, and is left with optic atrophy and a right hemiplegia. The literature concerning the neurotoxic effects of streptomycin is briefly reviewed.

We reviewed the clinical features of 12 patients with fat embolism seen in 10 years. Based on neurologic manifestations, patients were grouped into those with focal cerebral syndromes and those with diffuse encephalopathy. Patients with focal signs tended to present earlier with neurologic findings alone, did not have fever, and had less risk of pulmonary disorder than patients with encephalopathy.

A 69-year-old woman suddenly became comatose. Within 24 hours, she became lethargic, with a diffuse encephalopathy and no focal neurologic abnormalities. CT revealed a large, nondominant thalamic infarct.

• A previously healthy 58-year-old man had severe carbon monoxide poisoning. Following a comatose state, tics of the head, coprolalia, fits of shouting, and abnormal vocal utterances developed. In addition to the signs of diffuse encephalopathy, he had some of the features associated with idiopathic Gilles de la Tourette's syndrome. The computed tomographic scan showed ventricular enlargement and low-density areas in the basal ganglia.

To document possible changing characteristics of Sydenham chorea, we reviewed records of 240 patients with this diagnosis who were seen between 1951 and 1976. A dramatic progressive decline in the number of cases was observed. The syndrome occurred mainly in childhood. Female predominance was apparent only after the 10. There was a high femilial incidence for both chorea and rheumatic fever. Most patients had generalized chorea, and fewer than 20% had hemichorea. Dysarthria, probably of extrapyramidal origin, was frequent but neurologic abnormalities other than diffuse encephalopathy were rare. One-third of the patients had coexisting heart disease. Repeat attacks of Sydenham chorea occurred, but the recurrence rate was much less than noted in previous studies.

• A 59-year-old woman with a metastatic adenocarcinoma of unknown origin and no metabolic abnormalities developed a diffuse encephalopathy, with generalized triphasic waves seen on the electroencephalogram. Postmortem examination revealed widespread, multifocal perivascular carcinomatosis of the cerebral cortices. Triphasic waves have been described with dementing processes, subdural hematomas, and cerebrovascular disease, but they are more commonly seen with metabolic encephalopathies. This case demonstrates an additional nonmetabolic cause of triphasic waves.

IN A RECENT study of bulbar poliomyelitis1the conclusion was reached that many of the cerebral symptoms are secondary manifestations of anoxia2rather than the result of direct injury to the cortex by the virus. The present paper is a report on the histologic study of a fatal case in which peculiar psychic disturbances resulted from a severe diffuse encephalopathy, ostensibly of anoxic origin. REPORT OF CASE Clinical History. —M. P., a girl aged 10 years, was admitted to the pediatric service of the University of Kansas Medical Center (Dr. Herbert Miller), on July 26, 1946. On July 23 she had complained of sore throat and began to have a fever. A local physician gave her sulfonamide drugs, but her fever continued. On July 25 she began to vomit and complained of headache and stiffness of the neck, and her temperature rose to 102 F. (38.9 C.). No