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1.
New Iraqi Journal of Medicine [The]. 2013; 9 (1): 105-107
in English | IMEMR | ID: emr-127398

ABSTRACT

Cryptococcus neoformans is known as an opportunistic infection in patients with HIV and other immuncompromised states. Occurrence of cryptococcal infection in immunocompetent individuals is rare. Here we report a case of cryptococcal meningitis in an immunocompetent male, who presented to Emergency room with headache, vomiting, breathlessness and loss of consciousness


Subject(s)
Humans , Male , Immunocompromised Host , Immunocompetence , Hyperventilation/etiology , Hyperventilation/diagnosis , Opportunistic Infections
2.
J. bras. pneumol ; 35(7): 698-708, jul. 2009. ilus, tab
Article in English, Portuguese | LILACS | ID: lil-521399

ABSTRACT

Multiple respiratory abnormalities can be found in anxiety disorders, especially in panic disorder (PD). Individuals with PD experience unexpected panic attacks, characterized by anxiety and fear, resulting in a number of autonomic and respiratory symptoms. Respiratory stimulation is a common event during panic attacks. The respiratory abnormality most often reported in PD patients is increased CO2 sensitivity, which has given rise to the hypothesis of fundamental abnormalities in the physiological mechanisms that control breathing in PD. There is evidence that PD patients with dominant respiratory symptoms are more sensitive to respiratory tests than are those who do not manifest such symptoms, and that the former group constitutes a distinct subtype. Patients with PD tend to hyperventilate and to panic in response to respiratory stimulants such as CO2, triggering the activation of a hypersensitive fear network. Although respiratory physiology seems to remain normal in these subjects, recent evidence supports the idea that they present subclinical abnormalities in respiration and in other functions related to body homeostasis. The fear network, composed of the hippocampus, the medial prefrontal cortex, the amygdala and its brain stem projections, might be oversensitive in PD patients. This theory might explain why medication and cognitive-behavioral therapy are both clearly effective. Our aim was to review the relationship between respiration and PD, addressing the respiratory subtype of PD and the hyperventilation syndrome, with a focus on respiratory challenge tests, as well as on the current mechanistic concepts and the pharmacological implications of this relationship.


Múltiplas anormalidades respiratórias podem ser encontradas em pacientes com transtornos de ansiedade, particularmente no transtorno de pânico (TP). Indivíduos com TP experimentam ataques de pânico inesperados, caracterizados por ansiedade, medo e diversos sintomas autonômicos e respiratórios. A estimulação respiratória é um fenômeno comum durante os ataques de pânico. A anormalidade respiratória mais citada em pacientes com TP é a sensibilidade aumentada para o CO2, que originou a hipótese de uma disfunção fundamental nos mecanismos fisiológicos de controle da respiração no TP. Há evidências de que pacientes com TP com sintomas respiratórios predominantes são mais sensíveis a testes respiratórios do que aqueles sem a manifestação de tais sintomas, representando um subtipo distinto. Pacientes com TP tendem a hiperventilar e a reagir com pânico como resposta a estimulantes respiratórios como o CO2, gerando uma ativação de um circuito de medo hipersensível. Apesar de a fisiologia respiratória desses pacientes permanecer normal, algumas evidências recentes apontam a presença de disfunções subclínicas na respiração e em outras funções relacionadas à homeostase corporal. O circuito do medo, composto pelo hipocampo, córtex pré-frontal medial, amígdala e projeções do tronco cerebral, pode estar hipersensível em pacientes com TP. Essa teoria pode explicar porque os medicamentos e a terapia cognitivocomportamental são claramente eficazes. Nosso objetivo foi revisar a relação entre respiração e TP, especialmente o subtipo respiratório de TP e a síndrome da hiperventilação, focalizando os testes respiratórios, bem como as hipóteses mecanísticas e as implicações farmacológicas dessa relação.


Subject(s)
Humans , Panic Disorder/complications , Respiration Disorders/etiology , Carbon Dioxide/physiology , Disease Susceptibility , Hyperventilation/drug therapy , Hyperventilation/etiology , Hyperventilation/psychology , Panic Disorder/drug therapy , Respiration Disorders/drug therapy , Respiration Disorders/psychology
3.
Rev. chil. neurocir ; 19: 28-34, 2002. tab
Article in Spanish | LILACS | ID: lil-348518

ABSTRACT

Se diseña un protocolo de manejo de TEC pediátrico grave como un intento de unificar criterios de tratamientos a nivel nacional, desde el rescate hasta la UCI pediátrica. En la estructuración del protocolo se han considerado la revisión de la literatura y la experiencia de la UCI Pediátrica y el Servicio de Neurocirugía del Hospital Carlos van Buren de Valparaiso en el manejo de más de 400 TEC graves a través de 20 años. En el protocolo de distinguen dos líneas importantes: 1) el rescate, estabilización y traslado 2) el manejo en el centro terciario. Las medidas que se tomen durante el rescate y traslado son de vital importancia en el pronóstico definitivo. En esta etapa juegan un rol de vital importancia los equipos de rescate, los médicos de hospitales generales y los medios de traslado interhospitalario. Es fundamental que se tenga claro que hacer y que no hacer. En el manejo en la unidad de intensivo es necesario conocer los beneficios y riesgos de las terapias vigentes y las bondades y limitaciones de las técnicas de monitoreo. Pensamos que una estandarización en toda la secuencia de manejo puede ayudar a mejorar el pronóstico definitivo de los pacientes con TEC grave en nuestro medio


Subject(s)
Humans , Child , Clinical Protocols , Craniocerebral Trauma , Cerebrospinal Fluid , Craniotomy/methods , Craniocerebral Trauma , Health Facility Moving , Hemodynamics , Hyperventilation/etiology , Hypothermia, Induced , Prognosis , Hypertonic Solutions/adverse effects
5.
Braz. j. med. biol. res ; 32(11): 1389-98, Nov. 1999. ilus, graf
Article in English | LILACS | ID: lil-248433

ABSTRACT

Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (VE) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an NG-nitro-L-arginine methyl ester (L-NAME, 250 µg/µl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7 per cent inspired O2) caused hyperventilation and hypothermia in both control (from 541.62 + or - 35.02 to 1816.18 + or - 170.7 and 36.3 + or - 0.12 to 34.4 + or - 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 + or - 63.17 to 2670.29 + or - 471.33 and 36 + or - 0.12 to 35.3 + or - 0.12, respectively), but the increase in VE was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in VE or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.


Subject(s)
Animals , Male , Rats , Hyperventilation/etiology , Hyperventilation/physiopathology , Hypothermia/etiology , Hypothermia/physiopathology , Hypoxia, Brain , Locus Coeruleus/physiology , Nitric Oxide/physiology , Body Temperature , Enzyme Inhibitors/pharmacology , NG-Nitroarginine Methyl Ester/pharmacology , Rats, Wistar
6.
Rev. méd. Chile ; 127(2): 211-21, feb. 1999. ilus, tab
Article in Spanish | LILACS | ID: lil-243782

ABSTRACT

Patients with severe head injury are prone to pulmonary complications that result in hypoxemia or hypercarbia, which could worsen their neurological condition. A rational ventilatory approach requires a good knowledge of respiratory and neurological pathophysiology. Airway management is of prime importance in neurological patients. Prophylactic chronic hyperventilation in head trauma is no longer recommended since it could impair cerebral perfusion, although transient hypocarbia could be of benefit to some patients. The use of low or moderate positive and expiratory pressure levels apparently improves oxygenation without worsening intracranial pressure. Ventilatory management should be closely monitored and adjusted to hemodynamic, respiratory and neurological status to achieve a good outcome


Subject(s)
Central Nervous System Diseases/therapy , Respiration, Artificial/methods , Brain Injuries/complications , Brain Injuries/therapy , Ventilator Weaning , Central Nervous System Diseases/complications , Hyperventilation/etiology , Hyperventilation/physiopathology , Lung Diseases/etiology
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