Neurologic alterations in an HIV adult patient with pertussis: a case report.

BACKGROUND: Pertussis is a highly contagious disease of public health interest caused by the bacterium Bordetella pertussis. Although its incidence has decreased substantially after the introduction of a vaccination, the burden of the disease remains high. Although the paroxysmal phase is highly disabling, complications are uncommon and more prevalent in children than in adults. The most frequent neurological complication is encephalopathy, but seizures, paresis, paraplegia, ataxias, aphasias, and decerebration postures have also been described. The complication of decerebration postures has not been previously reported in adults. CASE PRESENTATION: We present a video case of an adult HIV patient with severe coughing paroxysms, post-tussive emesis and syncope, whose workup confirmed the diagnosis of a B. pertussis respiratory infection. During hospitalization, he had fluctuant encephalopathy and post-tussive decerebration postures following paroxysms. He was treated with antibiotic therapy and finally sent home without residual neurological deficits. CONCLUSION: This case illustrates the biological plausibility of neurologic complications of pertussis in adults, which, albeit rare, can cause important morbidities. Future research should explore whether there are differences in the clinical presentation, risk factors and pathophysiology of the disease among adults or interventions aimed at preventing or treating pertussis encephalopathy.

Vagal modulation of pre-inspiratory activity in hypoglossal discharge in the decerebrate rat.

Respiration consists of three phases--inspiration (I), post-inspiration (post-I), and late expiration (E2). Pre-I is a subphase occurring at the end of E2. Hypoglossal (XII) discharge contains I and occasionally pre-I activity. Functionally, XII pre-I underlies tongue muscle contraction and expansion of the upper airway, causing a decrease in airway resistance in anticipation of the succeeding inspiratory effort. It has been shown that vagotomy causes an increase in pre-I activity in XII in anesthetized animals. Also, in anesthetized artificially-ventilated animals, XII onset is synchronized with that of inspiratory phrenic nerve (PhN) activity. Therefore, we sought to systematically test the hypothesis that XII pre-I is present in vagus-intact unanesthetized decerebrate animals and vagal afferents negatively modulate XII pre-I discharge in decerebrate rats, in the absence of confounding anesthesia. Experiments were performed on seven Sprague-Dawley unanesthetized decerebrate adult male rats and bilateral PhN and XII recordings performed. In three animals, vagotomy was performed during PhN recordings and one animal was vagotomized during initial surgical preparation prior to recordings. In vagus-intact animals, XII pre-I duration averaged 12.4 ms. Vagotomy was associated with greater XII pre-I duration, expressed in absolute time (89.5 vs. 12.4 ms; p<0.01) as well as relative to the XII bursting period (18.9 vs. 3.4%; p<0.01). Vagal deafferentation was also associated with a larger relative amplitude of the pre-I XII activity relative to total XII discharge (12.4 vs. 2.1%; p<0.01). We conclude that pre-I discharge is present in vagus-intact artificially-ventilated unanesthetized decerebrate animals and is negatively modulated by vagal afferents.

Metabolic encephalopathies.

Kinnier Wilson coined the term metabolic encephalopathy to describe a clinical state of global cerebral dysfunction induced by systemic stress that can vary in clinical presentation from mild executive dysfunction to deep coma with decerebrate posturing; the causes are numerous. Some mechanisms by which cerebral dysfunction occurs in metabolic encephalopathies include focal or global cerebral edema, alterations in transmitter function, the accumulation of uncleared toxic metabolites, postcapillary venule vasogenic edema, and energy failure. This article focuses on common causes of metabolic encephalopathy, and reviews common causes, clinical presentations and, where relevant, management.

Rigidez de descerebración transitoria en el contexto de hipoxemia y administración de propofol, midazolamflumacenilo y remifentanilo-naloxona / No disponible

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Leptin responsiveness in chronically decerebrate rats.

Peripheral infusions of physiological doses of leptin decrease body fat mass, but it is not known whether this results from direct effects on peripheral tissue or activation of central leptin receptors. In this study, we infused chronically decerebrate (CD) rats, in which the forebrain was surgically isolated from the caudal brainstem, with 60 microg leptin/d or PBS for 14 d from ip mini-osmotic pumps. The CD rats were tube fed an amount of food equivalent to the intake of ad libitum-fed intact controls or 75% of this amount to account for their reduced energy expenditure. Control rats fed ad libitum or tube fed 75, 100, or 125% of their ad libitum intake also were peripherally infused with leptin or PBS. CD rats had a lower serum testosterone, energy expenditure, and lean body mass compared with controls but had increased levels of adiponectin and leptin and were obese. Leptin increased body fat and decreased energy expenditure during the light period in 100%-fed CD rats, but not 75%-fed CD rats. Leptin decreased body fat of ad libitum- and 100%-fed but not 75%-fed or 125%-fed intact controls. Energy expenditure did not change in any control group. These results show that leptin can change body fat independent of a change in food intake or energy expenditure, that the forebrain normally prevents leptin from inhibiting energy expenditure through mechanisms initiated in the caudal brainstem or peripheral tissues, and that the leptin response in both intact and CD rats is determined by the energy status of the animal.

Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets.

Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3-15 days. Blood pressure, end-tidal CO(2), body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by approximately 2.5 degrees C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR.

Incidência de cervicalgia e alterações posturais do segmento cefálico em pacientes portadores de DTM. Estudo retrospectivo / Incidence of cervicalgia and head postural changes in temporomandibular disorders patients. Retrospective analysis

Os autores estudaram a incidência de cervicalgia e de alterações posturais em pacientes portadores de DTM. Foram avaliados 307 pacientes (64 homens e 243 mulheres) no período de 1996 a 2002. Dos pacientes avaliados, 86,97% apresentaram dor na região cervical, 260 (84,69%) apresentaram anteriorização do segmento cefálico e 254 (82,74%) apresentaram protrusão dos ombros

Metallothionein I and II mitigate age-dependent secondary brain injury.

Both the immediate insult and delayed apoptosis contribute to functional deficits after brain injury. Secondary, delayed apoptotic death is more rapid in immature than in adult CNS neurons, suggesting the presence of age-dependent protective factors. To understand the molecular pathobiology of secondary injury in the context of brain development, we identified changes in expression of oxidative stress response genes during postnatal development and target deprivation-induced neurodegeneration. The antioxidants metallothionein I and II (MT I/II) were increased markedly in the thalamus of adult C57BL/6 mice compared to mice <15 days old. Target deprivation generates reactive oxygen species that mediate neuronal apoptosis in the central nervous system; thus the more rapid apoptosis observed in the immature brain might be due to lower levels of MT I/II. We tested this hypothesis by documenting neuronal loss after target-deprivation injury. MT I/II-deficient adult mice experienced greater thalamic neuron loss at 96 hr after cortical injury compared to that in controls (80 +/- 2% vs. 57 +/- 4%, P < 0.01), but not greater overall neuronal loss (84 +/- 4% vs. 79 +/- 3%, MT I/II-deficient vs. controls). Ten-day-old MT I/II-deficient mice, however, experienced both faster onset of secondary neuronal death (30 vs. 48 hr) and greater overall neuronal loss (88 +/- 2% vs. 69 +/- 4%, P = 0.02). MT I/II are thus inhibitors of age-dependent secondary brain injury, and the low levels of MT I/II in immature brains explains, in part, the enhanced susceptibility of the young brain to neuronal loss after injury. These findings have implications for the development of age-specific therapeutic strategies to enhance recovery after brain injury.

Atrophy responses to muscle inactivity. II. Molecular markers of protein deficits.

We examined the expression of several molecular markers of protein balance in response to skeletal muscle atrophy induced by spinal cord isolation (SI; i.e., a complete transection of the spinal cord at both a midthoracic and a high sacral level plus complete deafferentation between the two transection sites). This treatment nearly eliminates neuromuscular activity (activation and loading) of the hindlimb muscles while maintaining neuromuscular connectivity. SI was associated with a reduced transcriptional activity (via pre-mRNA analyses) of myosin heavy chain (MHC) and actin. In addition, there was an increased gene expression of enzyme systems impacting protein degradation (calpain-1; plus enzymes associated with polyubquitination processes) that could further contribute to the protein deficits in the SI muscles via degradative pathways. IGF-I receptor and binding protein-5 mRNA expression was induced throughout the 15-day period of SI, whereas IGF-I mRNA was induced at 8 and 15 days. These responses occurred in the absence of an upregulation of translational regulatory proteins (p70 S6 kinase; eukaryotic 4E binding protein 1) to compensate for the decreased protein translational capacity. These data collectively demonstrate that 1). the molecular changes accompanying SI-induced muscle atrophy are not necessarily the reverse of those occurring during muscle hypertrophy, and 2). the rapid and marked atrophy that defines this model of muscle inactivity is likely the result of multifactorial processes affecting transcription, translation, and protein degradation.

Atrophy responses to muscle inactivity. I. Cellular markers of protein deficits.

The goal of this study was to use the model of spinal cord isolation (SI), which blocks nearly all neuromuscular activity while leaving the motoneuron muscle-fiber connections intact, to characterize the cellular processes linked to marked muscle atrophy. Rats randomly assigned to normal control and SI groups were studied at 0, 2, 4, 8, and 15 days after SI surgery. The slow soleus muscle atrophied by approximately 50%, with the greatest degree of loss occurring during the first 8 days. Throughout the SI duration, muscle protein concentration was maintained at the control level, whereas myofibrillar protein concentration steadily decreased between 4 and 15 days of SI, and this was associated with a 50% decrease in myosin heavy chain (MHC) normalized to total protein. Actin relative to the total protein was maintained at the control level. Marked reductions occurred in total RNA and DNA content and in total MHC and actin mRNA expressed relative to 18S ribosomal RNA. These findings suggest that two key factors contributing to the muscle atrophy in the SI model are 1). a reduction in ribosomal RNA that is consistent with a reduction in protein translational capacity, and 2). insufficient mRNA substrate for translating key sarcomeric proteins comprising the myofibril fraction, such as MHC and actin. In addition, the marked selective depletion of MHC protein in the muscles of SI rats suggests that this protein is more vulnerable to inactivity than actin protein. This selective MHC loss could be a major contributor for the previously reported loss in the functional integrity of SI muscles. Collectively, these data are consistent with the involvement of pretranslational and translational processes in muscle atrophy due to SI.

Clinicoradiological observation in three patients with suicidal hanging.

STUDY DESIGN: A hospital-based clinical, radiological and neurophysiological study. OBJECTIVES: Hanging is a common mode of suicide in India, but there is paucity of MRI and neurophysiological findings in the context of clinical and neurological changes. We report the clinical, neurophysiological and MRI studies of three females who attempted suicide by hanging. METHODS: All three patients who attempted hanging underwent detailed clinical, electroencephalographic, motor, somatosensory and brainstem-evoked potential and magnetic resonance imaging studies. Patients were clinically followed up for 6 months. RESULTS: Their ages were 21, 26 and 35 years. They developed altered sensorium, decorticate posturing and had a wide variety of movement disorders. Patient no. 1 had the most severe illness and recovered by the seventh month while the others recovered earlier. MRI revealed hyperintense signal changes in the globus pallidus, caudate nucleus and thalamus in all patients and in the midbrain in one patient. Electroencephalography showed nonspecific slowing. Somatosensory, motor and brainstem-evoked potential studies were normal. CONCLUSION: Hanging leads to hypoxic brain damage resulting in signal changes mainly in the basal ganglia and thalamus and may be associated with transient movement disorders.

[Periodic decerebrate spasm with ocular dipping, Cheyne-Stokes respiration and hypersympathetic activity].

Decerebrate spasm is a generalized muscular spasm produced by some stimuli on decerebrate posture. Such spasm are called "tonic fit" or "decerebrate extensor spasm". We reported a 50-year-old man with periodic decerebrate spasm after cerebral hemorrhage. On admission, the patient was comatose. The pupils were round but anisocoric and did not react to light. Corneal reflexes were absent. The face, arms, and legs did not move voluntarily. Two weeks after admission, he was found in decerebrate rigidity. Periodic decerebrate spasms were also observed and were accompanied by ocular dipping. Cheyne-Stokes respiration, and hypersympathetic activity (transiently dilated pupils, hypertension, tachycardia). These symptoms persisted for two months and were induced by painful or sonic stimuli and suppressed by sleep, sedative or antiedematous drugs. The cycle was 0.6 approximately 0.7 per minute in accord with that of Cheyne-Stokes respiration. Magnetic resonance imaging revealed an area of low signal intensity in the midbrain to the bottom of the pons caused by the tentorial herniation on T1-weighted images. From the the clinical features and results of MRI studies, we considered that dysfunction of the midbrain to the pons in addition to diffuse cerebral dysfunction played some role in the manifestation of periodic decerebrate spasm with ocular dipping.

Phrenic nerve responses to lung inflation and hypercapnia in decerebrate dogs.

The effects of changes in static airway pressure (Paw) and arterial PCO2 (PaCO2) on phrenic nerve activity were studied in unanesthetized, decerebrate dogs and compared with previous results from chloralose/urethane anesthetized dogs using the same experimental preparation (Mitchell et al. 1982; Mitchell and Selby 1987). In ten mid-collicular decerebrate dogs, the lungs were independently ventilated while the left pulmonary artery was occluded and the right vagus nerve was transected. Changes in left lung Paw, therefore, exerted effects on pulmonary stretch receptors without altering blood gases; changes in the inspired gas ventilating the right lung controlled blood gas composition, without altering lung volume feedback. Phrenic burst frequency (f) and integrated amplitude (Phr) were monitored while Paw was varied between 2 and 12 cmH2O at various constant levels of PaCO2 between 31 and 69 mmHg. The major findings of this study are: (1) hypercapnia decreases the slope of the relationship between expiratory duration (tE) and Paw in both decerebrated and anesthetized dogs; (2) hypercapnia increases the inspiratory duration (tI) in decerebrated, but not anesthetized dogs; and (3) hypercapnia decreases the slope of the relationship between f and Paw due to these effects on tE and tI. These results support previous studies indicating that vagal and suprapontine mechanisms exert independent effects on respiratory timing. It is concluded that neither suprapontine influences nor anesthesia are necessary in the mechanism underlying interactions between stretch receptors and CO2-chemoreceptors in modulating tE. Furthermore, decerebration reveals a unique effect of CO2-chemoreceptors on tI, an effect found in anesthetized dogs only after carotid denervation.

Exertional rhabdomyolysis associated with decerebrate posturing.

A case is presented in which decerebrate posturing after a head injury led to rhabdomyolysis and renal failure. Exertional rhabdomyolysis is caused by an energy deficient state in overworked musculature that leads to a loss of integrity of the muscle cell. The resultant myoglobin in serum leads to acute renal failure. This condition should be suspected in a comatose patient with fever, brown discoloration of the urine, and edema of the extremities. Laboratory results will show orthotoluidine positive urine with a clear serum, elevated serum creatine phosphokinase, and serum creatinine elevation out of proportion to blood urea nitrogen. Management consists of fluids and diuretics with dialysis if necessary. Rhabdomyolysis with head injury and decerebracy may occur more frequently than has been previously reported.

Decerebrate posturing with the syndrome of inappropriate secretion of antidiuretic hormone.

Decerebrate and/or decorticate posturing have not yet been described as possible features of the syndrome of inappropriate secretion of antidiuretic hormone. Cerebral edema and loss of brain electrolytes are contributing factors resulting in altered excitability of the neural membrane. We describe a patient who, on the eighth day after a head injury, presented with decerebrate posturing, which coincided with the development of the syndrome of inappropriate secretion of antidiuretic hormone, and which rapidly reversed with the correction of the hyponatremia. We believe that the syndrome of inappropriate secretion of antidiuretic hormone should be included in the differential diagnosis of abnormal posturing in the head-injured patient.

[A comparison of the effects of baclofen and some other muscle relaxants on alpha-rigidity in rats].

Muscle relaxant effects of baclofen were compared with those of dantrolene, diazepam, chlordiazepoxide and tolperisone. When administered intraduodenally (i.d.), baclofen and dantrolene but not diazepam suppressed the sustained rigidity of forelimbs in anemically decerebrated rats, and ED50 values of the former two drugs were 2.9 and 22 mg/kg, respectively. Baclofen, dantrolene and diazepam reduced the phasic rigidity of the decerebrated animals induced by mechanical stimulation of hindlimbs, with their respective ED50 values of 6.2, 140 and 1.4 mg/kg, i.d. Both the rigidities were almost insensitive to chlordiazepoxide and tolperisone. With the exception of tolperisone, these drugs also produced a muscle relaxation in intact animals as measured by traction (rats), rotarod (mice), and grip-strength (mice) tests. ED50 or eD25 values were calculated to be in the following ranges: 5.6 approximately 12 mg/kg, p.o. for baclofen, 15 approximately 35 mg/kg, p.o. for dantrolene, 2.1 approximately 6.5 mg/kg, p.o. for diazepam and 33 approximately 64 mg/kg, p.o. for chlordiazepoxide. These results suggest that baclofen, unlike other drugs, may be effective in reducing both tonic and phasic rigidities at lower doses than those causing muscle relaxation in intact animals.

Metabolic changes in the hippocampus after prolonged epileptic discharge.

Sustained epileptic seizures were induced in cats by means of penicillin (PCN). After a three hour period tissue from the archicortex was removed, frozen, and extracted for metabolic studies. The concentration of ATP, ADP, AMP, phosphocreatine, glucose, glucose-6-phosphate, pyruvate, lactate, glutamate and aspartate were determined. There was a 50% decrease in phosphocreatine concentration, a slight decrease in the level of ATP and a slight increase in the levels of ADP and AMP. There was a decrease in the total adenine nucleotide and the ATP/ADP and ATP/AMP ratios. The absence of a significant change in adenylate energy charge potential reflects the remarkable ability of the brain to stabilize its energy state even after intense seizure activity. A reflection of increased glycolysis is the presence of decreased glucose (nearly 50%), and increased lactate, concentrations. The metabolic changes observed in the archicortex are comparable to those observed by others in the neocortex, indicating perhaps the relative metabolic uniformity of these two types of cortex.

Observations on the "dependent stage" of the "mirror focus".

The present communication was part of a larger study in which penicillin induced epileptogenic activity in the hippocampus of the "cerveau isolé cat" was investigated. The discharge contralateral to the side of the PCN focus, i.e., the mirror focus, was dependent upon the integrity of the commissural pathways. Interhippocampal latencies of bisynchronous epileptogenic discharge varied between 0 and 50 msec (mean 20). Interestingly the discharges could occur absolutely simultaneously and even more surprising, the mirror focus discharge occasionally led that in the primary focus! An interpretation as to how this might occur is given.

[Formation of an epileptic complex in the cerebral cortex and effect of diazepam on it with different levels of cerebral transection]. / Obrazovanie épilepticheskogo kompleksa v kore golovnogo mozga i vliianie na nego diazepama pri razlichnykh urovniakh pererezki mozga.

Effect of diazepam on the activity of the epileptic complex consisting of a number of foci created with strychnine applications to the brain cortex under conditions of intact brain and at different levels of it neuronal isolation was studied in acute and chronic experiments on cats. It was shown that in the preparations of cerveau isolé and cortex isolé a more rapid formation of the epileptic complex under the influence of the determinant focus, and marked generalizaiton of convulsant activity could be observed. Diazepam induced a decrease in the amplitude and frequency of convulsive discharges. There was a break in the synchronization of their appearance first in the dependent foci and then in the determinant one. The diazepam effects were seen both in the intact brain and in the preparations of cerveau isolé and cortex isolé. These findings indicate that diazepam may exert an indirect action on the brain cortex that does not exclude the participation of other brain structures in the realization of the diazepam effect under conditions of intact brain.