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[Isaacs' syndrome. Report of a case and review of the literature].
The case of a 17-year-old boy who had been well until the age of four when progressive stiffness of lower limbs developed is reported. Soon walking became difficult and on on his thighs, buttocks and calves one could notice the appearance of myokymia. Painful and intermittent spasms were often present specially after physical strain. This was followed by profuse sweating. Strength was normal but muscle relaxing was slow mainly in the quadriceps. The familiar history for neuromuscular pathology was negative. Muscle enzymes, thyroid function tests were within normal limits and muscular biopsy showed no abnormalities. The EMG disclosed a permanent spontaneous activity, more evident in the quadriceps, which was normal in shape, amplitude and duration. In association to this activity multiplets discharges and low motor units were also observed; in interferencial pattern appeared at maximum contraction but the multiplets and low motor units potentials kept on showing even though voluntary muscular activity ceased. The therapeutic essay with carbamazepin had a dramatic effect upon the course of the patient's conditions. He showed a great improvement with this drug and today leads a normal life being able even to play soccer and ride a bicycle. An interesting remark which should be done is the fact that the flexion of the neck inhibits the quadriceps myokymia whereas the extension makes them to appear and even worsen. Unfortunately is was not possible to carry out a more accurate investigation concerning electropharmacology and hystopathology as the patient was uncooperative and refused to undergo such examinations. However the authors believe that this clinical picture can be considered as a case of "continuous muscle-fibre activity" due to the great similarity it bears to the cases related by Isaacs in 1961. An extensive review concerning the pertinent literature has been done.
Syndrome of continuous muscle fiber activity. Case report with 11-year follow-up.
A 16-year-old male patient who presented with muscle stiffness and dysphonia is described. Electromyography revealed continuous motor activity that was unaffected by peripheral nerve block or general anaesthesia, but was abolished by curare. The patient had a marked improvement after using phenytoin. The follow-up 11-years later corroborates with the proposed benignity of this syndrome, in spite of being dependent on medication.
Severe hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with fluoxetine: case report.
Hyponatremia is a significant complication of treatment with serotonin selective reuptake inhibitors (SSRI). We describe a case of a 53-year-old woman that was started on fluoxetine 20 mg/day for depression. Nine days later, the patient started with weakness, nausea, progressing to confusion, inappetence and vomit. Three hours later she became unresponsive and had a generalized seizure. She was brought to our emergency service. On admission, the patient was normovolemic, without focal motor deficits, but had mild generalized muscle rigidity and Babinski's sign bilaterally. Serum sodium was 105 mmol/L, serum osmolality, 220 mmol/L, and urinary osmolality, 400 mmol/L. The other laboratory exams, chest X-ray, cerebrospinal fluid and cranium tomography were normal. She was found to have fluoxetine-induced SIADH and it was discontinued. We started the hyponatremia correction and, in 5 days, the mental status of the patient gradually returned to a normal baseline, paralleling the resolution of her hyponatremia, without recurrence. Hyponatremia and SIADH should be considered if a patient experiences deterioration in his or her clinical condition while taking SSRI. The use of SSRI antidepressants should be remembered in the differential diagnosis of drug-induced hyponatremia.
Acute lithium intoxication and neuroleptic malignant syndrome.
A 45-year-old man was admitted to our hospital after taking an intentional overdose of 90 sustained-released lithium tablets (450 mg each). The patient was stabilized with three sessions of hemodialysis. On day 7 of his hospital stay, his serum lithium level was 0.5 mEq/L. On day 10, he developed high fever, tachypnea, muscle rigidity, rhabdomyolysis, acute renal insufficiency, mental confusion, and obtundation. His creatine kinase level was 698 IU/L, serum creatinine 3.5 mg/dl. Late-onset neuroleptic malignant syndrome (NMS) was diagnosed. The patient died after developing acute renal failure and acute respiratory distress syndrome. Clinicians should be aware that lithium may cause NMS independent of other neuroleptic agents.
Olanzapine-associated neuroleptic malignant syndrome.
Neuroleptic malignant syndrome (NMS) is a rare but potentially serious complication of neuroleptic drugs. It may vary in both presenting characteristics and severity. Several different criteria for diagnosis exist, and each differs from the others slightly. We describe a 66-year-old woman with chronic paranoid schizophrenia who was prescribed olanzapine along with several other psychiatric drugs and an antihypertensive drug. The patient displayed several characteristics of NMS during therapy with olanzapine, including fever, elevated creatine kinase level, leukocytosis, and mild muscle rigidity. When olanzapine was held, the signs and symptoms improved and then returned with rechallenge of olanzapine. For this reason, olanzapine was considered strongly associated with this patient's apparent NMS episode. The patient's beta-blocker therapy may have masked additional signs of NMS. In addition, the patient tolerated other neuroleptics that were started in the hospital after the suspected NMS episode. The variation among different diagnostic criteria makes this syndrome a challenging diagnosis at times, in particular when atypical antipsychotics are suspected as the causative agent.
The neuroleptic malignant syndrome and acute renal failure.
Rhabdomyolysis is a clinical disorder arising from skeletal muscle injury. Many potentially fatal complications may develop after rhabdomyolysis, including hyperkalemia, disseminated intravascular coagulation, and acute renal failure. Both traumatic and nontraumatic causes of rhabdomyolysis are seen. Frequently, nontraumatic rhabdomyolysis is associated with the use of common drugs. We report such a case--a patient afflicted with the neuroleptic malignant syndrome (NMS). NMS is characterized by fever, muscle rigidity, and neurologic changes after treatment with neuroleptic agents such as haloperidol. These symptoms may progress to rhabdomyolysis and acute renal failure. Many similar disease entities, especially those that display hyperpyrexia, resemble NMS. Thus, the diagnosis should rest on pertinent history as well as the recognition of these relevant clinical signs. Treatment should be directed toward averting the systemic complications of drug-induced rhabdomyolysis and renal failure. Discontinuation of the neuroleptic medication is imperative. Aggressive iv hydration, systemic and urine alkalinization, and therapy for life-threatening electrolyte abnormalities are all appropriate additional therapeutic goals. The use of dantrolene or bromocriptine may hasten recovery from NMS. Although mortality from NMS alone is unusual, NMS with concomitant renal failure carries a worse prognosis. The treatments outlined here may avert progressive renal failure and reduce mortality in patients with NMS-induced rhabdomyolysis and renal failure.
Real-time measurement of frozen gait in patient with parkinsonism using a sensor-controlled walker.
Patients with Parkinson's disease develop gait disturbances. Although the use of walkers is very effective for maintaining locomotive ability, patients who have symptoms such as frozen gait (FG) and festinating gait may fall even with a walker equipped with a brake as they cannot use the brake well in an emergency and fail to follow the accelerating walker. None of the studies on walking aids to date have addressed real-time detection of FG or the use of this information for the control of the walking aid, monitoring of the state of improvement in the ambulatory function, or evaluation of the effect of the use of a walker. In this study, we evaluated whether the state called FG, a characteristic symptom of Parkinson's disease, can be detected by the use of a sensor-controlled walker with heel-to-toe pressure sensors. The following two measurements were carried out in one male healthy and a one male patient with stage 3 Parkinson's disease by the Hoehn-Yahr scale showing mild muscle rigidity, hypokinesia, and FG. In the healthy subject, the heel-to-toe pressure showed smooth heel-to-toe shifts during the standing phase. In the patient with Parkinson's disease, the heel-to-toe response time was about 2.4 times longer than in the healthy subject at the beginning of walking, and FG could be recorded as the difficulty in lifting the foot by the toes. Also, when FG was observed during walking, the pressure waves recorded by the same sensors showed two peaks occurring at short interval, indicating double landings.
Neuroleptic malignant syndrome. Recognition, prevention and management.
Neuroleptic malignant syndrome (NMS) is a rare but potentially lethal form of drug-induced hyperthermia characterised by mental status changes, muscle rigidity, hyperthermia and autonomic dysfunction. Increased awareness and early recognition will lead to prompt management. The diagnosis of NMS presents a challenge because several medical conditions generate similar symptoms. The presentation and course of NMS can be quite variable ranging from a stormy and potentially fatal course to a relatively benign and self-limiting course. The most important aspect of treatment is prevention. This includes reducing risk factors (e.g. dehydration, agitation and exhaustion), early recognition of suspected cases and prompt discontinuation of the offending agent. All patients with psychosis should be monitored daily for dehydration and elevated temperature, have vital signs checked and agitation should be watched for. Antipsychotics should be used conservatively with gradual titration of doses. The management of NMS should be based on a hierarchy of symptom severity. Following an episode of NMS, the patient should be reassessed for further treatment with antipsychotics and rechallenge should not be attempted at least 2 weeks following resolution of symptoms of NMS. The patient and family should be educated about the episode and consent for further medication use obtained after a clear explanation of the risk-benefit analysis.
Tremor-predominant Parkinson's disease. Approaches to treatment.
Parkinson's disease is a neurodegenerative disorder that manifests clinically with variable degrees of tremor, muscle rigidity, bradykinesia and postural instability. Tremor-predominant Parkinson's disease is characterised by prominent tremor of one or more limbs with a relative lack of significant rigidity and bradykinesia. Despite the lack of other disabling motor symptoms, the tremor of tremor-predominant Parkinson's disease can be very disabling, especially if a postural and kinetic component exists. A wide variety of treatments for Parkinson's disease tremor are currently available and include use of oral medications, injections with botulinum toxin and neurosurgical procedures. Some of the first line medications (levodopa, dopamine agonists, anticholinergics) are very effective in controlling tremor. However, some patients with Parkinson's disease tremors are unresponsive to first line drugs and treatment with second line medications (clozapine, amantadine, clonazepam, propranolol, neurontin) should be attempted. In the small number of patients with disabling tremor that is refractory to all medications, neurosurgical intervention should be considered. Both thermocoagulation and deep brain stimulation at several different neuroanatomical sites (thalamus, globus pallidus, subthalamic nucleus) offer good to excellent tremor control with relatively low risk to the patient.
Antidepressant toxicity and the need for identification and concentration monitoring in overdose.
Antidepressant drugs are among the most commonly encountered causes of self-poisoning. These drugs include tricyclics, tetracyclics, bicyclics and monocyclics, as well as monoamine oxidase (MAO) inhibitors and selective serotonin reuptake inhibitors (SSRIs). Of these, the tricyclic antidepressants (TCAs) are generally more toxic in overdose, with major toxicity usually manifesting within the first 6 hours after overdose. Various studies indicate that patients at risk of toxicity from TCA overdose may be identified by neurological, cardiovascular and electrocardiography status, together with a quantitative estimate of the plasma drug concentration. While there are various methods available for such chemical estimations, the most satisfactory appears to be fluorescence polarisation immunoassay which gives rapid quantitative results for a variety of TCAs. The selective MAO-A inhibitor antidepressants and the SSRIs are relatively nontoxic when taken alone. However, overdoses of combinations of MAO inhibitors and either SSRIs or TCAs with serotonin reuptake blocking activity may result in a serotonin syndrome with a severe or fatal outcome. Features of this syndrome include hyperpyrexia, disseminated intravascular coagulation, convulsions, coma and muscle rigidity, which may not develop until 6 to 12 hours after overdose. While quantitative chemical identification of these drugs following overdose is helpful in confirming the diagnosis, it is not mandatory. The increasing use of MAO-A inhibitors and SSRIs in the treatment of depression suggests that careful clinical observation is required when combination overdoses are suspected.
Successful treatment of levodopa-induced neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) in a patient with Parkinson's disease.
After 9 years of treatment for Parkinson's disease, a 68-year-old woman developed the complications of neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) while she was still receiving levodopa, bromocriptine and amantadine hydrochloride. The patient displayed a high fever (40 degrees C), impaired consciousness, marked systemic muscle rigidity, tremor and bloody stools. The diagnosis of NMS and DIC was made on the basis of the symptoms and the results of blood serological tests. The antiparkinsonian drugs that had been administered until her admission to our hospital were continued unchanged, while the NMS was treated with dantrolene sodium and the DIC, with nafamostat mesilate. Both of the above-mentioned therapies were effective. The present case is rare in that the patient developed NMS and DIC during treatment and not after the discontinuation of the antiparkinsonian drugs.
Type 1 diabetes mellitus and drug-resistant epilepsy: presence of high titer of anti-glutamic acid decarboxylase autoantibodies in serum and cerebrospinal fluid.
A 55-year-old man who was diagnosed as having type 1 diabetes mellitus (DM) at the age of 50 years was started on insulin therapy. At 54 years old of age, he suddenly developed complex partial seizures, which frequently occurred despite intensive anti-epileptic drug therapy. Neurological examination on admission revealed hyporeflexia in bilateral upper and lower extremities without any muscle rigidity, painful spasm or cerebellar ataxia. Laboratory examination showed poor glycemic control with increased glycated hemoglobin levels. Positive anti-thyroglobulin antibodies and anti-thyroid peroxidase (TPO) antibodies and slight elevation of TSH levels are consistent with subclinical hypothyroidism due to Hashimoto's thyroiditis. A high titer of anti-glutamic acid decarboxylase (GAD) antibodies was detected in the patient's serum and cerebrospinal fluid (CSF). Electroencephalography showed temporal spikes, consistent with complex partial seizure. This is a very rare case presenting with concomitant type 1 diabetes and drug-resistant epilepsy associated with high titers of circulating and CSF anti-GAD antibodies.
Parkinsonism in cerebrotendinous xanthomatosis.
This report describes a case of cerebrotendinous xanthomatosis (CTX) accompanied by clinical manifestations of parkinsonism, including oily and masked face, marked akinesia, muscle rigidity and resting hand tremor. Magnetic resonance imaging (MRI) of the brain showed high intensity areas on T2 weighted imaging, and slightly low intensity areas on T1 weighted imaging in the right globus pallidus and the left putamen. Cerebral cortical atrophy with slight ventricular dilatation and cerebellar atrophy were present as well. This is a case report of CTX which manifested parkinsonism. Parkinsonism may not be a coincidental manifestation in CTX, but rather represent a symptom of the same underlying diathesis.
Effect of L-dopa on electromyograph and heart rate of parkinsonians.
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Unstable fractures in children with acute, severe brain injury.
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[A case of interval form of carbon monoxide poisoning with a remarkable recovery].
A 69-year-old woman was admitted to our hospital due to an interval form of carbon monoxide (CO) poisoning one month after acute CO poisoning. On admission, she had disorientation, memory disturbance, apathy, masked face, muscle rigidity, bradykinesia and parkisonian gait. An MRI (FLAIR image) revealed high signal intensity lesions in the bilateral globus pallidus and the white matter of the frontal lobe. Hyperbaric oxygen (HBO) therapy at 2 atmospheres for 60 min was given every day, in addition to citicoline, levodopa/DCI and selegiline hydrochloride. Cognitive disturbance and parkinsonism gradually decreased, and abnormal signals in the bilateral globus pallidus and the cerebral white matter were attenuated after the treatment. Neuropsychiatric abnormalities except for a slight gait disturbance disappeared one and a half month after starting the treatment. In addition to HBO therapy, administration of citicoline, lovodopa and selegiline may be useful in the case of the interval form of CO poisoning.
Stereotaxic surgery for cerebral palsy.
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