Cases reported "Hyperventilation"

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1/16. epilepsy in vacuolating megalencephalic leukoencephalopathy with subcortical cysts.

    Vacuolating megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a disorder characterised by acquired macrocephaly, developmental motor delay of varying degrees, slowly progressive cerebellar and pyramidal signs, and initially preserved intellectual function. More than 60% of the published cases had epileptic seizures. In this study, we analysed the seizures and EEG findings of nine patients with MLC. Six patients (66.6%) with moderate to severe neurological impairment had epilepsy, four with partial and two with generalised seizures. The EEG of five epileptic patients revealed epileptogenic foci over the temporal, frontal and parietal regions with variable predominance during waking and sleep. The facilitation of spike-and-wave paroxysms by eye closure, by intermittent photic stimulation and by hyperventilation were determined in four patients. Four patients also showed abnormalities in the background activity. In conclusion, we think that epilepsy is a significant component of MLC compared to the other leukodystrophies. The elucidation of the underlying molecular defect may explain the unusual pathogenetic relation between this leukoencephalopathy and the associated seizures.
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2/16. A case of adversive seizures induced by hyperventilation.

    We report a case of adversive seizures featuring neck rotation and conjugate deviation induced by the hyperventilation maneuver. At the age of 6 years the patient suffered from conjugate deviation to the left. She herself felt no symptoms other than oculomotor symptoms. hyperventilation induced an adversive seizure and ictal EEG showed sharp waves in the right frontal, central, and parietal areas. No brain image showed abnormal findings. Zonisamide completely attenuated her attacks. It is well known that hyperventilation induces absence seizures, and it has been reported that hyperventilation can induce complex partial seizures. However, no previous reports have described patients diagnosed as having adversive seizures with conjugate deviation induced by hyperventilation. We report the present case because, although its epileptogenesis is unknown, the patient is a rare case not only clinically but also electrophysiologically.
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3/16. Mimics of coronary heart disease.

    Numerous disorders can mimic chronic coronary disease either clinically or electrocardiographically. Particularly noteworthy are wolff-parkinson-white syndrome, asymmetric septal hypertrophy, floppy mitral valve syndrome, angina pectoris with normal coronary arteries, hyperventilation syndrome, neurogenic T wave abnormalities, vasoregulatory abnormality, cervicoprecordial angina, hyperkalemia or hypokalemia, left ventricular hypertrophy, and left anterior fascicular block.
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4/16. Pulmonary hyperinflation and respiratory distress following solvent aspiration in a patient with asthma: expectoration of bronchial casts and clinical improvement with high-frequency chest wall oscillation.

    An 18-year-old student with a history of asthma accidentally inhaled organic solvent during a class, with immediate cough and dyspnea that worsened over several hours. He presented in severe respiratory distress, with hypoxemia and marked pulmonary hyperinflation. Administration of inhaled bronchodilator was ineffective because of agitation, and the patient could not be positioned for chest physiotherapy to treat presumed widespread mucus plugging. High-frequency chest wall oscillation (HFCWO) in the sitting position initially caused increased distress but was subsequently tolerated when noninvasive positive-pressure ventilation (NPPV) via nasal mask was initiated. Almost immediately, the patient began expectorating bronchial mucus casts, with concomitant clinical improvement. Endotracheal intubation was avoided, and with aggressive pharmacologic treatment for acute severe asthma and continuation of intermittent HFCWO-NPPV, the patient made a full recovery over the next several days. This case suggests that the combination of HFCWO and NPPV may be helpful in the presence of mucus plugging as a complication of acute inhalation injury or acute severe asthma.
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5/16. Cyanotic episodes in a male child with fragile x syndrome.

    A 9-year-old male with a diagnosis of fragile x syndrome (FXS) was evaluated for cyanotic episodes of unknown etiology. Clinical observation revealed frequent episodes of hyperventilation lasting several minutes, only while the patient was awake. This was followed by apnea associated with cyanosis and oxygen desaturation. Polysomnogram confirmed episodic central apnea temporally associated with hypocapnia, only during the awake state. Extensive evaluation failed to reveal other neurological, cardiac, gastrointestinal, or pulmonary etiologies for the events. The clinical observations and investigations allowed us to conclude that the patient's cyanotic episodes were caused by primary behavioral hyperventilation in the awake state. Similar behaviors have been reported in children with a variety of diagnoses but to our knowledge have not been previously reported in children with FXS. Treatment for this unusual behavior in FXS consists of reassurance and behavior modification to decrease the frequency and severity of the cyanotic episodes.
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6/16. parietal lobe source localization and sensitivity to hyperventilation in a patient with subclinical rhythmic electrographic discharges of adults (SREDA).

    OBJECTIVE: Subclinical rhythmic electrographic discharges of adults (SREDA) is currently considered a benign EEG pattern of uncertain significance. The underlying cortical sources and generating mechanisms are unknown. We performed a source localization analysis of SREDA with the aim of better understanding this unusual EEG pattern. methods: Multiple spontaneous episodes of typical SREDA were recorded in a patient during continuous EEG monitoring. Additional SREDA episodes were induced by hyperventilation. Source localization was carried out using statistical non-parametric mapping (SNPM) of low resolution electromagnetic tomography (LORETA). RESULTS: SNPM of both time- and frequency-domain LORETA revealed a widespread biparietal cortical origin of SREDA, the anatomical distribution of which included the parietal operculum and the known vascular watershed areas between anterior, middle and posterior cerebral arteries. Vigorous deep hyperventilation induced SREDA on three of four attempts. Mean duration of the hyperventilation-induced SREDA was approximately three times longer than spontaneous events. CONCLUSIONS: Investigations in this patient with typical SREDA revealed hyperventilation sensitivity and a posterior hemispheric source localization maximal in the parietal cortex bilaterally, in large part overlying the anatomical distribution of the vascular watershed areas. SIGNIFICANCE: The source localization results and sensitivity to hyperventilation suggest some sort of association between cerebral vascular supply and SREDA, as originally proposed by Naquet et al. [Naquet R, Louard C, Rhodes J, Vigouroux M. A propos de certaines decharges paroxystiques du carrefour temporo-parieto-occipital. Leur activation par l'hypoxie. Rev Neurol 1961;105:203-207.].
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7/16. Emotional effects on seizure occurrence.

    Emotional factors can alter the likelihood of seizure occurrence, and they usually increase the frequency of attacks. Our case studies showed that such activation is brought about through missed medication, sleep deprivation, and hyperventilation. Less well documented is the possibility that increased excitability and seizures may be due to direct neuronal activation of limbic circuits, although such a mechanism would be quite plausible.
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8/16. Pseudoseizures caused by hyperventilation resembling absence epilepsy.

    During the 4-year period, 1982-1986, 18 patients presented to the Children's Hospital, Camperdown, Sydney, with the following features: (1) Recurrent "absences" clinically indistinguishable from childhood absence epilepsy, (2) Normal clinical examination, (3) Electroencephalogram (EEG) demonstrating normal waking background and sleep activity. On hyperventilation, "absences" occurred, characterized on EEG by a marked build-up of paroxysmal slow-wave activity unassociated with evidence of epileptic activity. We designate these attacks "pseudoseizures caused by hyperventilation resembling absence epilepsy." Individual cases demonstrated a variety of other symptoms consistent with the hyperventilation syndrome. There was an identifiable environmental stress in 13 of the 18 cases. Follow-up of 13 patients after a mean period of 20 months revealed that only two children continued to have occasional absences, associated with a clear history of breathing up when upset. Treatment did not influence outcome. On repeat hyperventilation with EEG and respiratory monitoring, five of the 13 had pseudoseizures. There was no indication that susceptibility to these episodes was associated with an abnormal CO2 response. It is postulated that the occurrence of pseudoseizures is related to cerebrovascular immaturity and an excessive vasoconstrictor response to a given level of CO2.
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9/16. Non Q-wave myocardial infarction following hyperventilation test.

    We report a case of acute myocardial infarction following a hyperventilation test performed at coronary angiography. The potential pathophysiological mechanisms and clinical implications are discussed.
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10/16. High incidence of primary cerebral lymphoma in tumor-induced central neurogenic hyperventilation.

    An awake patient presented with central neurogenic hyperventilation induced by a cerebral tumor. Corticosteroid therapy and brain irradiation while the patient was anesthetized and respiration controlled under pancuronium-induced respiratory paralysis were followed by tumor regression and resolution of hyperventilation. recurrence of tumor 6 weeks later was not accompanied by recurrence of hyperventilation. Cytologic study of cerebrospinal fluid revealed B-cell lymphoma. This patient brings to 10 the number of cases recorded with tumor-induced central neurogenic hyperventilation. Five of the eight patients with known tumor histology had a primary cerebral lymphoma, a rare neoplasm that comprises only 1% of all intracranial neoplasms. The disproportionately high frequency of central neurogenic hyperventilation in patients with cerebral lymphoma has therapeutic implications that are briefly reviewed.
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