Rc Jiloha

Kleine-Levine syndrome in an adolescent female and response to modafinil

Kleine-Levine Syndrome (KLS) is a disorder characterized by a triad of periodic hypersomnia, hyperphagia, and hypersexuality. KLS, although more common in young males, it has also been seen in females. Treatment options available for its management include mood stabilisers like lithium, stimulants like amphetamines, antidepressants and other options including electroconvulsive therapy. Modafinil is one of the new stimulant medications approved for narcolepsy. Herein, we report a young female with KLS and showing favorable response to modafinil. More data is required to establish the effectiveness of modafinil in this syndrome.

Tardive Meige's syndrome associated with olanzapine

Meiges syndrome is characterized by blepharospasm and oromandibular dystonia. It has been reported as a complication of typical antipsychotics. To the best of our knowledge, case of olanzapine-induced tardive Meiges syndrome has not been reported in the literature. We we are reporting report a case of Meiges syndrome developing after long term therapy with olanzapine.

Trihexyphenidyl (benzhexol) in clozapine-induced nocturnal enuresis and sialorrhea

Sir, Clozapine is an atypical antipsychotic medication. It is the agent of choice to treat patients with schizophrenia who are treatment-resistant and who are prone to extrapyramidal symptoms. However, besides occasional serious and life-threatening side effects like agranulocytosis, myocarditis, and seizures, clozapine is often discontinued because of many common and troublesome side effects like sialorrhea, sedation, weight gain, and nocturnal enuresis in up to 17% of patients.[1] Clozapine-induced sialorrhea occurs at rates varying from 10 to 80% as reported in the literature.[2] Nocturnal enuresis is a less commonly reported side effect with a reported frequency varying from as little as 0.23% to as high as 41%.[3,4]

Olanzapine induced tardive dystonia.

Advent of atypical antipsychotics was thought to be a major advancement in the psychopharmacology for schizophrenia. It was thought that these drugs would have low propensity to induce extrapyramidal symptoms including tardive movements. Olanzapine is a thienobenzodiazepine derivative, second generation (atypical) antipsychotic agent. Compared to typical antipsychotics, it has a greater affinity for serotonin 5-HT2A than dopamine D2 receptors, with preferential action at mesolimbic than nigrostriatal dopaminergic pathways. However, only few reports of olanzapine induced tardive dystonia (TD) are available in the literature. We wish to report another case of TD, in a male patient with schizophrenia, which developed after 15 months of treatment with olanzapine.

Subacute sclerosing panencephalitis presenting as mania

Subacute sclerosing panencephalitis (SSPE) is a rare, invariably fatal degenerative disease of the central nervous system developing after measles infection. Besides neurological symptoms as initial presenting symptoms, rare reports of its presentation with pure psychiatric symptoms have been reported. We here report a case of 14 year old male who initially presented with manic symptoms and then subsequently diagnosed to be suffering from SSPE. Improtance of ruling our organic conditions is emphasized.

Amisulpride induced mania.

Amisulpride is an atypical antipsychotic used for the management of schizophrenia and other conditions like dysthymia. It has also been used for the management of bipolar disorders as an add on therapy. Here, we report a patient of schizophrenia who developed a manic episode while on amisulpride.

Quetiapine induced myoclonus

Miss D, a 19-year-old female presented to us with history suggestive of manic episode for the last 2 months. Her past history also revealed history of 2 GTCS around 6 years back for which no treatment was sought. Her family and personal history were non signiÞ cant. She was started on quetiapine gradually increased to 300 mg per day over a week and lorazepam 2 mg at night. She showed improvement in her symptoms over the next 2 weeks. After this, the dose was increased to 400 mg per day. After 2 days of this, she developed sudden abrupt jerks lasting for less than a second, especially involving the right upper extremity. These movements would at times be so frequent that she even dropped the things in her hand. An EEG revealed intermittent bilateral polyspike discharges. Her biochemical investigations and MRI brain were normal. The dose of quetiapine was decreased to 200 mg per day and after about 1 week the patient did not have these jerky movements. EEG after 10 days of this was normal. Quetiapine was then stopped and she was started on oxcarbamazepine and lorazepam and improved in 1 month.

Breast enlargement associated with low dose olanzapine.

Sir, Olanzapine, an atypical antipsychotic agent, is not commonly associated with significant hyperprolactinemia due to its weak dopamine binding capacity.[1] Previous reports suggested that olanzapine might be a safe alternative treatment for cases with antipsychotic induced hyperprolactinemia.[2,3] It has little effect on prolactin levels and is generally regarded to be prolactin sparing, although at higher doses hyperprolactinemia may result.[4,5] Contrary to this, we wish to report a case of olanzapine-induced breast enlargement secondary to hyperprolactinemia in a woman with obsessive compulsive disorder (OCD) at a low dose of 5 mg/day. A 40-year-old married female presented with a history suggestive of OCD for last 20 years. She was treated with a number of antiobsessive drugs in adequate doses and for adequate duration but with minimal response. Her past and family histories were not significant. Personal history revealed interpersonal problems with husband and her in-laws. The patient was started on a combination of clomipramine and sertraline. Clomipramine was increased to a dosage of 275 mg/day and sertraline to 200 mg/day. However, with this combination, the patient did not show significant clinical response. The compliance was adequately ensured and the combination was continued for 4 months at the same dosage. Simultaneously, behavior therapy in the form of exposure and response prevention was started. The patient, however, did not cooperate for behavior therapy as, at times, there was no co-therapist available, and on other occasions, the patient did not comply with the instructions given. As a result, olanzapine at a dose of 5 mg/day was added to the existing treatment. After about 2 months of addition of olanzapine, the patient came for follow-up with complaints of bilateral enlargement of the breasts. The enlargement was diffuse, symmetrical, non tender without galactorrhea. She also had amenorrhea for 2 months. Investigations revealed serum prolactin level increased to 97 ng/mL (normal range = 1.5–19.0 ng/mL). Magnetic resonance imaging of the brain did not show any evidence of microadenoma. Other hematological investigations like complete blood count, liver function tests, blood urea, serum creatinine, glucose tolerance test and thyroid function tests (T3, T4 and TSH) were within normal limits. Her pregnancy test was negative. There was no other significant finding on general physical or systemic examination. There was no family history of breast related disorders. Olanzapine was stopped and patient was monitored for the next 1 month. Serum prolactin level estimated after 1 month of drug discontinuation was 25 ng/mL. Her menstrual cycles regularized after 2 months but there was no improvement in her breast enlargement. Subsequently, the patient was referred to surgery department where breast reduction surgery was performed. The breast tissue removed weighed around 2.5 kg and its histopathology revealed hypertrophy of glandular tissue. Her prolactin level was checked again after 2 months of surgery and was 10 ng/mL. Buspirone at a dose of 30 mg/day was added and the patient showed some improvement in her symptoms with addition of buspirone to a combination of clomipramine and sertraline. In view of the temporal correlation between the initiation of olanzapine and development of breast enlargement and elevation of prolactin levels and return to normal prolactin levels subsequent to olanzapine withdrawal, olanzapine seems to be the likely causative agent. The score on Naranjo adverse drug scale was 6, suggesting a probable relationship with the drug.[6] Other causes of hyperprolactinemia like pregnancy, thyroid disorders, acromegaly, pituitary microadenoma, etc.[7] were ruled out on the basis of normal investigations and no abnormal findings on general and systemic examination. The histopathological examination of the breast tissue also did not reveal any other pathology. Olanzapine has been tried for augmentation in patients with OCD.[8] However, peculiarities of our case included the fact that the patient was only on 5 mg/day of olanzapine and that the patient had to undergo a major operation for the side effect which was distressing to the patient. Our report suggests that one should be cautious while prescribing antipsychotic agents to non psychotic patients who might be more sensitive to the side effects of these medications. Also, to the best of our knowledge, the literature search did not reveal any report of bilateral breast enlargement due to hyperprolactinemia with olanzapine. Bilateral breast enlargement as a consequence of hyperprlactinemia has not been reported.[9,10] We hope our clinical experience with olanzapine stimulates additional systematic clinical trials to reveal the magnitude of such side effects.

Aripiprazole for olanzapine-induced symptomatic hyper prolactinemia

Sir, Aripiprazole is a novel atypical antipsychotic medication as it is a potent dopamine partial agonist and also acts as a partial agonist at serotonin (5-HT)1A and as an antagonist at 5-HT2A receptors.[1] It has been theorized that dopamine partial agonists may be able to stabilize the dopaminergic system without inducing a hypo dopaminergic state, thereby reducing the risk of side effects associated with pure blockade of dopamine receptors, especially extra pyramidal and endocrinological side effects. We hereby report a patient in whom addition of aripiprazole to ongoing treatment with olanzapine resulted in resolution of olanzapine induced hyper prolactinemia. The patient: A 29-year-old married female suffering from schizophrenia since three years. Her illness was characterized by suspiciousness, muttering to self, violent, aggressive behavior and disturbed biological functions. There was no significant past or family history of any psychiatric or neurological illness. She was initially treated with risperidone and haloperidol, each in adequate dose and for adequate duration, without much response. Her family members did not agree to clozapine fearing that they would not be able to monitor the blood counts. Subsequently, she was started on olanzapine up to 20 mg per day and gradually started showing improvement in symptoms. She was maintaining well when she decreased the dose on her own and subsequently had exacerbation of her symptoms. As a result, olanzapine was increased to 25 mg per day. After about one month of this therapy, the patient started reporting breast tenderness with milky discharge from nipples. She also reported scanty menstruation. At this time, her serum prolactin level elevated and was at 47 ng / mL (normal: 1.5–19.0 ng / mL). Ancillary tests, including thyroid profile and brain computed tomography scan, were normal. In view of past non response to antipsychotic drugs, olanzapine was continued in the same dose and aripiprazole was added to olanzapine in the dose of 15 mg per day. After two weeks of this addition, her serum prolactin level was 27 ng / mL. After about a month of this, the patients symptoms improved completely and her prolactin level was within the normal range (11 ng / ml). The patient has been maintaining well on this combination for the last six months. There are similar reports, of combining aripiprazole with risperidone and with haloperidol to offset hyper prolactinemia.[2,3] Paradoxically, there are also reports of aripiprazole causing galactorrhea.[4,5] and not being effective in treatment of hyper prolactinemia associated with antipsychotic medication.[6] Although a switch to aripiprazole is an understandable and probably useful strategy, it might not be clinically useful to switch to another antipsychotic when a patient has responded to the medication. Our case did not respond to a previous trial of risperidone and haloperidol and it was not clinically feasible to stop or taper olanzapine. Perhaps these apparent inconsistencies may be reconciled by considering that aripiprazole is a partial agonist, thereby it may act as either an agonist or an antagonist depending upon the conditions. The partial agonist property of this compound means that in the presence of dopamine hypo activity, as induced by olanzapine, aripiprazole functions as a dopamine agonist with roughly 30% intrinsic activity at postsynaptic receptors,[1] restoring tonic inhibition to anterior pituitary lactotrophs. Spontaneous prolactin decline in this case would be unlikely because the time since olanzapine exposure was short. Our report suggests that aripiprazole might be useful as an add-on therapy in patients who develop hyper prolactinemia as a side effect to another antipsychotic without affecting the clinical outcome.