Lichen planus induced by carbamazepine: a case report

We report a case of Lichen planus in a female patient who has been treated for epilepsy in the Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia. She was diagnosed with mesio-temporal lobe epilepsy with secondary generalization and had been treated for years with carbamazepine. In Novemeber 2009, erythematous papulosquamous papules were noticed on her trunk and under her breasts which spread to her legs. Dermatohistological testing confirmed the diagnosis of Lichen planus. Replacement of carbamazepine with oxcarbazepine and application of steroid therapy resulted in regression of skin changes.     

Hyperammonemia in asterixis induced by carbamazepine: two case reports

Two patients developed asterixis while they were taking carbamazepine at "therapeutic" levels. The only laboratory abnormality was slight hyperammonemia. It occurred with normal hepatic function as a dose-related effect. In fact, the blood ammonia level decreased and asterixis ceased when carbamazepine was stopped or reduced in dosage. The relationship between asterixis and hyperammonemia during carbamazepine therapy is discussed.     

A case of cranial fasciitis induced by trauma]

We present a 20-month-old boy with a rapid growing occipital mass after head trauma, that was pathologically diagnosed as cranial fasciitis. Cranial fasciitis, first described as a specific entity by Lauer and Enzinger in 1980, is a benign fibroblastic lesion occurring in children that resembles nodular fasciitis pathologically. Nodular fasciitis also shows benign proliferation of fibroblasts and myofibroblasts in the subcutaneous tissues. This disease was firstly reported in 1955. This lesion is arising in the upper and lower extremities and trunk in adult commonly. The rapid growth, abundant cellularity, and mitotic activity cause these lesions to be misdiagnosed as sarcomas frequently. However, these lesions recur rarely, do not develop metastases, and are readily cured only by surgical excision. Cranial fasciitis is similar to nodular fasciitis in clinical cause and pathology. Therefore cranial fasciitis should be considered a variant of nodular fasciitis, although it differs from noduler fasciitis in its frequent site and age. Cranial fasciitis occurs in skull bone and in childhood. The cause of them are still unknown. However, we speculate on the relationship between head trauma and cranial fasciitis making reference to the fact that 5-15% of nodular fasciitis were caused by trauma. So we investigated this relationship in cranial fasciitis, then 8 cases of 40 cases(20%), that we could trace in the world literatures, had histories of previous head trauma. From this result, head trauma is one of a cause of cranial fasciitis probably.     

Mental disorders induced by carbamazepine

We present here a case with various physical and neuropsychiatric symptoms caused by the administration of carbamazepine. The patient suffering from right ophthalmic neuralgia showed fever, eczema, erythema, lymphoadenopathy, eosinophilia, vomiting, headache, dizziness, nystagmus, and various mental disorders which consisted of emotional instability, personality change, delusions of reference and persecution, depressive state, and hyperventilation syndrome during the administration of carbamazepine. The physical symptoms in the present case were conformable to the side effect of carbamazepine. The mental disorders appeared in a few days from the start of carbamazepine administration and disappeared after the discontinuation of the administration of this drug without antipsychotic therapy and have never relapsed until now. The mental disorders and the physical symptoms were in parallel with their clinical course. This kind of mental disorders induced by carbamazepine has not yet been reported.     

A case of carbamazepine intoxication with alpha coma and status epilepticus]

We report a 14-year-old girl with carbamazepine intoxication who developed alpha coma and status epilepticus. She fell into deep coma and developed frequent generalized convulsions. The EEG during coma showed diffuse alpha activity predominantly in the frontal area. Serum carbamazepine concentration was 42.8 micrograms/ml. The convulsions were suppressed by diazepam only transiently, and by midazolam completely. Although half a day had passed since carbamazepine ingestion, we could wash out much of drug remnants by gastric lavage. Thereafter, the serum concentration of carbamazepine decreased efficiently and the patient recovered dramatically without complication. Early diagnosis and appropriate treatments should improve the prognosis of carbamazepine intoxication.     

A case of parkinsonism induced by an oral contraceptive]

We report a case of parkinsonism induced by long term administration of an oral contraceptive. A 38-year-old woman complained of easily stumbling, démarche à petit pas and fatiguability in her lower extremities since January, 1991. When examined on April 5, 1991, she explained taking an oral contraceptive for 7 years on her doctor's recommendation after two times artificial abortions. Her facial expression was mask-like and body was bent forward with knee joints flexed and arms flexed at elbow joints. She had frozen gait with inactive pendulousness of the arms. We could find her muscle rigidity in both upper and lower extremities, especially in her right side extremities. A brain MRI finding was lacunar infarction which proton density weighted and T2-weighted MR images showed small patches of high-signal intensities in white matter of the bilateral frontal lobes and in left periventricular white matter. Her symptoms improved after stopping administration of the oral contraceptive and starting combination therapy with nicergoline and bromocriptine. She had some leg fatiguability at the onset of her next menstruation in May, but it was much less than her previous condition. When her menstruation terminated, those symptoms disappeared and it was possible to stop the administration of bromocriptine and nicergoline, and her symptoms have improved.     

A case of polymyalgia rheumatica with improved steroid-responsibility after discontinuing carbamazepine]

A 70-year-old woman under anticonvulsive therapy with carbamazepine and valproate was diagnosed as polymyalgia rheumatica. She responded to the prednisolone therapy so poorly that she required high dose prednisolone and methotrexate, and it was difficult to reduce prednisolone. After discontinuing of carbamazepine, her steroid response improved immediately. Carbamazepine is known to induce hepatic enzyme CYP3A4 and alter metabolism of other drugs. In our case, the effect of prednisolone might have been reduced by carbamazepine. This case suggests more attention should be paid to the interaction between carbamazepine and prednisolone.     

Asterixis induced by carbamazepine therapy.

There are very few reports about asterixis as a side effect of treatment with psychopharmacologic agents. In this report we present four patients treated with a combination of different psychotropic drugs, in whom asterixis was triggered either by adding carbamazepine (CBZ) to a treatment regimen, or by increasing its dosage. Neither dosage nor serum levels of CBZ were in a higher range. We consider asterixis to be an easily overlooked sign of neurotoxicity, which may occur even at low or moderate dosage levels, if certain drugs as lithium or clozapine are used in combination with CBZ.     

A case of superior sagittal sinus thrombosis following long-term medication with carbamazepine]

A 55-year-old man, who had been medicated with carbamazepine, phenobarbital, and sodium valproate for 12 years' duration, presented with severe headache, nausea, and transient diplopia. The neurological examination revealed mild disturbance of consciousness and postural tremor. He also complained of severe continuous headache but no throbbing pain. Enhanced head CT showed empty delta sign and irregular pooling of contrast agent around the superior sagittal sinus. Head MRI did not show the flow void in the superior sagittal sinus. Cerebral angiography demonstrated incomplete occlusion of the superior sagittal sinus and well-developed colateral channels. He was diagnosed having superior sagittal sinus thrombosis, and was placed on anticoagulant and antiplatelet drugs. He did not have any other risk factors such as inflammatory disease, infection, malignancy, and oral contraceptives. However, he had been medicated with some anticonvulsants including carbamazepine, which is known to induce venous thrombosis in the leg. Therefore, the association between superior sagittal sinus thrombosis and long term medication with carbamazepine was suspected. This is the first case report of anticonvulsant-associated cerebral venous thrombosis. It suggests that long-term medication with carbamazepine should be considered to be one of the risk factors for cerebral venous thrombosis.     

A case of Parkinson's disease with neuroleptic malignant syndrome induced by paroxetine]

We present a first case of Parkinson's disease with neuroleptic malignant syndrome by Paroxetine, one of the selective serotonin reuptake inhibitor (SSRI). The patient was a 73-year-old woman who had been diagnosed as Parkinson's disease for one and half year. The severity of her disease was categorized as Hoehn & Yahr 2nd degree and she had taken 0.25 mg/day of Pramipexole. Four days after the addition of 10 mg/day of Paroxetine for the treatment of her depression, she developed consciousness disturbance, severe muscular rigidity, tremor, fever, hyperhidrosis, incontinence and elevated serum creatine kinase level. According to diagnostic criteria, she was diagnosed as neuroleptic malignant syndrome probably induced by Paroxetine. Her clinical symptoms and laboratory data were improved seven days after intravenous drip infusion. We should recognize that SSRI could induce neuroleptic malignant syndrome in patients with Parkinson's disease.     

A case of brain stem infarction with bilateral hearing loss]

The study case was a 66-year-old man who had bilateral neurosensory hearing impairment due to brain stem infarctions. He noticed mild hearing loss, frequent vertigo and tinnitus. About one month later, his hearing took a sudden turn for the worse, and he suffered from dysarthria, dysphagea and abasia. Neurological examination revealed pseudobulber palsy, left hemiparesis, cerebeller ataxia, disturbance of pain and temperature sensation on the right face and left side of the body. Brain stem auditory evoked potentials (BAEPs) showed a delayed small wave V with the abscence of previous waves on the right side and no significant waves on the left side. Brain magnetic resonance images (MRI) revealed infarctions in the bilateral middle cerebellar peduncles, including in the right lateral portions of pons, and the right lower pontine base. We believe that not only peripheral, but also central auditory pathways adjacent to infarctions were damaged. Magnetic resonance angiography (MRA) showed severe stenosis or occlusion of left vertebral artery and basilar artery. We concluded that hypoperfusion of the vertebrobasilar artery territories caused ischemia of the cochlear nerve and the auditory tracts in the brain stem, which resulted in bilateral hearing loss.     

Distigmine bromide induced Parkinsonism. A case report]

A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without laterality. T2 weighted MRI showed mild front-temporal atrophy and multiple hyperintensities in both deep white matters. His symptoms fully improved one week after discontinuance of distigmine bromide. This is the first case report of distigmine bromide induced Parkinsonism.     

A case of musicogenic epilepsy induced by listening to an American pop music]

This is the second report of musicogenic epilepsy in Japan. A 23-year-old woman was admitted to our hospital due to the musicogenic epilepsy. She had four generalized tonic clonic seizures at 18 and 19 years old. Since 19, she had had complex partial seizures lasting for about 20 seconds which was easily evoked by listening to an American pops particularly "Dreamlover" song by Mariah Carey. Brian MRI and interictal 99mTc HMPAO-SPECT showed no abnormalities. In the ictal EEG recording, three minutes after listening to the song, seizure activities were recorded from the right temporal region with 11Hz rhythmic epileptiform activities over the right temporal region and subsequent delta activities over the right hemisphere. The song that induced the seizure had a specific meaning that might evoke her emotion as had been pointed out in the previous reports.     

A case of hypoxic brain damage induced by severe asthma successfully treated by hypothermia therapy]

We experienced a case of hypoxic brain damage induced by severe asthma who was successfully treated by hypothermia. A 20-year-old woman with a history of bronchial asthma suffered from severe respiratory distress and she stopped breathing for about 20 minutes. She was admitted to our hospital with respiratory arrest, deep coma, mydriasis and weak motor response to pain. She was intubated and mechanically ventilated with 100% oxygen. She was cooled down to 33 degrees C within 4 hours of her arrival. Her body temperature was maintained at about 33 degrees C for 2 days, and then gradually rewarmed. During hypothermia, PaCO2 was quite high(80-100 mmHg), but the intracranial pressure was kept low. After hypothermia therapy, she became free from consciousness disturbance and there were no neurological disorders except for mild myoclonus. Hypothermia has a possibility of effective therapy for patients with hypoxic brain damage after respiratory distress.