Hemiplegic migraine episode triggered by regadenoson.

SPECT and PET myocardial perfusion imaging (MPI) are widely used to evaluate patients for coronary artery disease. Regadenoson (a selective A2A adenosine receptor agonist) is a commonly used vasodilator agent for stress MPI because of its safety profile and ease of use. Common adverse reactions such as headache, shortness of breath, flushing, and chest and abdominal discomfort are typically mild and can be effectively reversed using methylxanthines such as aminophylline and caffeine. Neurological adverse reactions such as seizure and stroke have rarely been reported with the use of regadenoson. The hemodynamic changes associated with regadenoson administration, such as an exaggerated hypotensive or hypertensive response, may be the cause for the reported cerebrovascular accidents. Activation of central nervous system A2A adenosine receptors is thought to be responsible for seizure episodes in patients with or without known histories of seizure. A2A adenosine receptors activation is also believed to play a role in headaches and migraine. This patient reported who has a history of hemiplegic migraine developed left side weakness and headache following the administration of regadenoson during a PET MPI study. Imaging work-up to rule out cerebrovascular accident was normal. After 1 hour from the onset of his symptoms, his weakness and headache significantly improved with complete resolution within 24 hours. We concluded that regadenoson triggered a hemiplegic migraine episode in this patient, which has not been previously reported in the literature. It may be prudent to avoid regadenoson and adenosine use in patients with a history of hemiplegic migraine.

The muscle findings in a pediatric patient with live attenuated oral polio vaccine-related flaccid monoplegia.

A pediatric patient, who was given live-attenuated oral polio vaccine twice without distinct gait disturbance during infancy, begun to present limp at 3 years. His gait disturbance became remarkable with aging. At 7 years, he was unable to dorsiflex the left ankle, and presented flaccid monoplegia of the left lower extremity, and the left Achilles tendon reflex was diminished. Magnetic resonance imaging revealed multiple crack-lines in the left anterior tibial muscle, but was unable to detect any distinct lesion at responsible level of L4, L5 and S1 anterior horn cells' degeneration. Electromyography showed continuous fibrillation potentials, but muscle biopsy presented nearly normal in this muscle. The serum levels of polio antibody type 1 and type 2 titers were elevated 64× respectively, while the type 3 antibody titer was not elevated 4×. This patient was diagnosed as live attenuated oral polio vaccine-related flaccid monoplegia, with mild clinical course.

Monoplegia after combined spinal epidural anesthesia.

Serious neurological complications after neuraxial block, including permanent neurological injury, are rare in contemporary anesthetic practice. We report a case of a 36 year old female undergoing a venous stripping operation under combined spinal epidural anesthesia (CSE). The CSE procedure was completed after a second attempt at the L4-L5 level and the surgery was completed uneventfully. After full recovery of motor block in the recovery room, the patient was discharged to the surgical ward. Epidural patient controlled analgesia with levobupivacine 0.125% and fentanyl 2 µg/ml was initiated. 10 hours after surgery, right lower limb sensory loss and monoplegia occurred. The epidural catheter was removed and normal MRI findings were noted. After one month of physical therapy treatment and two months follow up the patient was able to walk with the aid of a walking stick. We discuss factors that might have contributed to radiculopathy and neurotoxicity as a cause of neurologic deficit.

Immune reconstitution inflammatory syndrome associated with PML in AIDS: a treatable disorder.

An HIV-1-infected patient with progressive multifocal leukoencephalopathy presented clinical deterioration and contrast-enhancing lesions on brain nuclear MR after the initiation of highly active antiretroviral therapy (HAART). Brain biopsy identified an inflammatory reaction compatible with immune reconstitution inflammatory syndrome. Treatment with corticosteroids and transient suppression of HAART led to marked neurologic improvement.

Etomidate speech and memory test (eSAM): a new drug and improved intracarotid procedure.

BACKGROUND: The intracarotid amobarbital procedure (IAP) is an important part of comprehensive investigation of patients who are candidates for surgical treatment of epilepsy. Owing to repeated and lengthy shortages of amobarbital, causing delays in elective surgery, attempts have been made to find a suitable alternative anesthetic. The authors report their experience using etomidate, a widely used agent for the induction of anesthesia. METHODS: Sixteen consecutive patients requiring IAP to evaluate memory or to lateralize speech underwent the procedure using etomidate. Prior to the procedure a catheter was placed in the internal carotid artery and an angiogram was performed. EEG was recorded and read online by an electroencephalographer. An anesthetist injected the drug, administered by bolus followed by an infusion, which was maintained until each speech measure had been sampled and new memory items had been introduced. The infusion was then stopped and testing continued as in a standard IAP. RESULTS: In all cases (30 hemispheres) contralateral hemiplegia followed injection. EEG slow waves were observed in every injected hemisphere, with some contralateral slowing anteriorly in 18. Global aphasia with preserved attention and cooperation followed dominant-hemisphere injections. These phenomena remained during infusion, and upon its termination returned gradually to baseline over a period of about 4 minutes. CONCLUSIONS: Etomidate is a viable alternative to amobarbital, and its administration by bolus followed by infusion offers an improvement over the traditional intracarotid amobarbital procedure. Cognitive tests can be performed during an assured hemianesthesia of the injected hemisphere.

Effect of tumor necrosis factor antagonism on allergen-mediated asthmatic airway inflammation.

OBJECTIVE: To assess whether tumor necrosis factor (TNF) antagonism can attenuate eosinophilic airway inflammation in patients with mild-to-moderate allergic asthma. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: National Institutes of Health (NIH) Clinical Center. PATIENTS: Twenty-six patients with mild-to-moderate allergic asthma, receiving only inhaled beta-2-agonists, who demonstrated both an early and late phase response to inhalational allergen challenge. INTERVENTION: Injection of a soluble TNF receptor (TNFR:Fc, etanercept, Enbrel) or placebo, 25mg subcutaneously, twice weekly for 2 weeks, followed by a bronchoscopic segmental allergen challenge. MEASUREMENTS: The primary outcome measure was whether TNFR:Fc can access the lung and inhibit TNF bioactivity. Secondary outcome measures included pulmonary eosinophilia, Th2-type cytokines, and airway hyperresponsiveness. RESULTS: Anti-TNF therapy was associated with transient hemiplegia in one patient, which resulted in suspension of the study. Data from the 21 participants who completed the study were analyzed. Following treatment, patients receiving anti-TNF therapy had significantly increased TNFR2 levels in epithelial lining fluid (ELF) (P<0.001), consistent with delivery of TNFR:Fc to the lung. TNF antagonism did not attenuate pulmonary eosinophilia and was associated with an increase in ELF IL-4 levels (P=0.033) at 24h following segmental allergen challenge. TNF antagonism was not associated with a change in airway hyperresponsiveness to methacholine. CONCLUSIONS: TNF antagonism may not be effective for preventing allergen-mediated eosinophilic airway inflammation in mild-to-moderate asthmatics. Transient hemiplegia, which may mimic an evolving stroke, may be a potential toxicity of anti-TNF therapy.

Acute methotrexate neurotoxicity: findings on diffusion-weighted imaging and correlation with clinical outcome.

BACKGROUND AND PURPOSE: Acute lymphocytic leukemia (ALL) is a common malignancy of childhood treated with methotrexate (MTX), which is associated with acute neurotoxicity. We evaluated diffusion-weighted (DW) and conventional MR images in children with ALL and acute MTX-induced neurotoxicity, with clinical correlation. METHODS: Five patients aged 12-15 years underwent fluid-attenuated inversion recovery (FLAIR), T2-weighted fast spin-echo and gradient-echo, T1-weighted gadolinium-enhanced spin-echo, and DW imaging within 24 hours of symptom onset. Records were reviewed for the temporal relationship to MTX administration, strokelike symptoms, and neurologic outcome. RESULTS: Six strokelike events were temporally related to intrathecal MTX given 6-11 days before symptom onset. FLAIR images showed abnormal hyperintensity in the callosal splenium in one patient but were otherwise normal. Diffusion abnormalities were frontoparietal in three events and frontal in one; nonfluent aphasia was seen in all. Bilateral frontoparietal diffusion abnormalities were associated with bilateral upper-extremity weakness, right-sided hemiparesis, or left-sided hemiparesis (one patient each); one patient had mild facial droop. Unilateral precentral subcortical diffusion abnormality was associated with contralateral motor deficit and ipsilateral upper-extremity sensory loss. Strokelike symptoms resolved rapidly and were not associated with other signs of encephalopathy. Subsequent intrathecal MTX administration was not associated with recurrence in four patients. CONCLUSION: Diffusion abnormalities in acute MTX neurotoxicity indicated cerebral dysfunction but not necessarily overt structural injury to the cerebrum. Subsequent demyelination or gliosis could not be predicted on the basis of diffusion abnormalities. A single strokelike episode with diffusion abnormalities should not necessarily prompt modification of potentially curative chemotherapeutic regimens.

Neuroleptic malignant syndrome associated with olanzapine therapy: a case report.

We present the case of a 42-year-old male with a history of schizophrenia who developed signs and symptoms consistent with Neuroleptic Malignant Syndrome (NMS) after 3 weeks of treatment with Olanzapine. The patient presented with hyperpyrexia, tremors, labile blood pressure, and mental status changes that had progressed over the preceding 24 h. Laboratory data revealed a metabolic acidosis and an escalating creatinine phosphokinase. Olanzapine is a relatively new atypical anti-psychotic agent first introduced in November of 1996 under the trade name of zyprexa. Olanzapine differs from typical anti-psychotic agents in that it has a lower affinity for dopaminergic receptors and binds antagonistically to serotonin receptors in the nigrostriatal pathway. These unique properties result in relatively fewer extra-pyramidal symptoms when compared to traditional anti-psychotics. Because of olanzapine's favorable side-effect profile, it has quickly gained popularity in the psychiatric community. Although NMS is a recognized complication of anti-psychotic use, there has been only one case of olanzapine induced NMS reported in the literature. The POISON-INDEX system, used by toxicologists throughout the United States, does not list NMS as a potential reaction to olanzapine. The pharmacists at our institution were also unaware that NMS was a possible complication of olanzapine. We present this case to make clinicians aware of the potential for Olanzapine induced NMS.

Hemiplegia following general anaesthesia: an unusual presentation of migraine.

We report the case of a 33-year-old woman who developed a dense hemiplegia immediately after an uncomplicated general anaesthetic for diagnostic laparoscopy. She had a history of recurrent hemiplegic migraine with a strong family history. Her migraine was normally associated with visual disturbances and a unilateral headache followed by a left-sided weakness such that she was unable to walk. Symptoms would last up to 24 h. Her post-operative state was atypical of her normal migraine, in that she had no headache or visual disturbance and initially all four limbs were affected.

Ischemic stroke following an intramuscular injection of diclofenac. Case report.

Nonsteroidal antiinflammatory drugs (NSAIDs) have arterial vasospastic properties. The authors report a stroke that occurred within minutes following an intramuscular injection of diclofenac. A sixty-one-year-old man, a heavy smoker, was admitted for an acute onset of mild hemiparesis thirty minutes after a single intramuscular injection of diclofenac. The neurologic deficit was resolved at one month of follow-up. The authors suggest a temporal causal relationship between the cerebrovascular event and the injection of diclofenac. The mechanism of stroke might be related to a synergistic vasospastic property shared by the use of an NSAID and heavy smoking.

[Neurologic complications during chemotherapy of children with acute lymphoid leukemia]. / Központi idegrendszeri szövödmények akut lymphoid leukaemiás gyermekek chemotherapiás kezelése során.

The case histories of two patients with acute lymphocytic leukemia, who developed central nervous system complication during combined chemotherapy are described. The neurological picture could be characterized by symptoms of headache, mental deterioration, hemiparesis and seizures. Following L-asparaginase administration one patient had intracranial thrombosis with focal seizures and hemiparesis associated with clotting abnormalities, including severe hypofibrinogenemia and decreased antithrombin III activity. In the other patient, it was after intrathecal administration of Methotrexate when mental deterioration associated with the symptoms of progressive leukoencephalopathy occurred. It arises the possibility that with increasing complexity of combined chemotherapy the occurrence rate of neurological complications will also increase.

Hemiparesis and ischemic changes of the white matter after intrathecal therapy for children with acute lymphocytic leukemia.

Three children with acute lymphocytic leukemia (ALL) developed delayed-onset transient hemiparesis and facial palsy after intrathecal (IT) administration of methotrexate (MTX) alone or as part of triple intrathecal chemotherapy for central nervous system (CNS) prophylaxis. The hemiparesis developed 10 to 14 days after IT therapy. Two of three children also experienced transient, profound expressive dysarthria. These episodes occurred during maintenance treatment after multiple IT administrations and without previous CNS toxicity. Two of three children received intermediate-dose MTX, 1 g/m2, not less than 5 weeks before events. These patients had not received cranial irradiation and had no evidence of CNS leukemia before or after these episodes. Ischemic changes on computerized tomographic scan or magnetic resonance imaging studies were documented in all three cases. Such changes are unusual manifestations of neurotoxicity in children after intrathecal therapy.

Cerebral infarct precipitated by praziquantel in neurocysticercosis--a cautionary note.

A patient who developed a cerebral infarct during the course of praziquantel therapy for neurocysticercosis is described. Destruction of a large number of cysts by praziquantel followed by a massive inflammatory response was likely to have precipitated the event. Caution on the use of this drug in patients with heavy parasite loads is emphasized.

Hemiplegia and focal convulsions as a manifestation of cyclosporine A toxicity.

Hemiplegia and focal convulsions were observed in a patient who received cyclosporine A after bone marrow transplantation. Cessation of the drug resulted in prompt reversal of the symptoms. The diagnostic problems and implications of this case are discussed.

Central neurotoxicity following intracarotid BCNU chemotherapy for malignant gliomas.

Central neurotoxicity is reported in 5 of 16 patients with recently diagnosed anaplastic gliomas, who received intra-arterial BCNU (200 mg/M2/course) and also 2 in a series of 26 patients with recurrent gliomas similarly treated. Neurotoxicity was usually delayed, commencing several weeks following the second or third course. CT scans during central neurotoxicity represented 1 or more of 3 patterns: no change; increased low density area(s); and/or ipsilateral gyral enhancement and punctate calcification in the middle cerebral artery territory. In one clinicopathological correlation, coagulative necrosis of the white matter was observed, identical histologically to those changes recognized as delayed vascular events following radiotherapy. Cautious exploration of the various clinical factors that may contribute to this toxicity seems appropriate, as exploration of the potential benefits of regional chemotherapeutic infusions is undertaken.