[Depressive disorders in primary care: Clinical features and sociodemographic characteristics]. / Troubles dépressifs en soins primaires : caractéristiques cliniques et sociodémographiques.

INTRODUCTION: Our aim was to determine the reason for consultation and the clinical features of depressive disorders according to the diagnostic and statistical manual (DSM) 4th edition IV R in primary care and to identify if there is an association between sociodemographic characteristics and depressive pattern. MATERIALS AND METHODS: In a cross-sectional study conducted to determinate the prevalence of depressive disorders in primary care, at three urban centers in two cities Salé and Oujda by five physicians, we recruited primary care 396 patients of whom 58 were depressed, among these patients we screened for depressive disorders, their clinical features, the melancholic characteristics and suicidal ideation using the Mini International Neuropsychiatric Interview. RESULTS: Mean age of the 58 depressive patients was 46±15 years. They were predominantly female, inactive and of low socio-economic level. Approximately one-third of the patients were illiterate and single. The symptoms frequently encountered were sadness (63.7%), anhedonia (62%), insomnia (45.7%), anorexia (60.9%), psychomotor retardation (60.9%) and asthenia (73.9%). Somatic symptoms were present 99%, the most common complaint was pain that exhibited 68.6% prevalence. Suicidal ideations were found in 36.2% of these depressive patients. CONCLUSION: The accuracy of the clinical features of patients with depression in primary care will facilitate the detection of these disorders by general practitioners and improve management of depression.

[Hysterical pseudo-coma: A case report]. / Le pseudo-coma hystérique: à propos d'un cas clinique.

Hysterical pseudo-coma corresponds to a state of clinical sleep with contrasting waking electroencephalogram. It can last several hours or even several days in the absence of an underlying organic disease. In psychiatry, this disorder is currently part of the "dissociative disorder not otherwise specified". Through this case report, we describe the evolution of a hysterical pseudo-coma that lasted four days in a 28-year-old man. The normality of biological, radiological and electroencephalographic assessments, and responsiveness of the patient during the implementation of a nasogastric tube, led us to suspect a mental origin. An adapted psychiatric care allowed the patient to recover his autonomy after three days of hospitalization. This had prevented the escalation of explorations and invasive treatments. However, the search for organic comorbidity and its management remains a priority.

[Antipsychotic-induced priapism and management challenges: a case report]. / Priapisme sous antipsychotiques et défis de prise en charge: à propos d'un cas.

INTRODUCTION: Priapism is a persistent, and often painful, penile erection, lasting more than 3 hours, not usually associated with sexual stimuli. It is a urological emergency that can cause serious complications. Drugs are responsible of the onset of 25 to 40% of cases of priapism. Several classes of medication are involved: antidepressants, antihypertensives, anticoagulants, alpha-blockers and some psychoactive substances (alcohol, cocaine, cannabis...). However, about 50% of drug related priapism is due to antipsychotics (AP). Clinicians should be aware of this rare side effect because of the severity of its complications and the difficulty of its management, especially in non-stabilized psychotic patients. CASE REPORT: We report a case of a 22-year-old male Moroccan patient, diagnosed with schizophrenia, who had been admitted for the first time to a psychiatric hospital for management of a psychotic episode. First, he received 15 mg per day of haloperidol, and seven days later he developed priapism. The patient was immediately referred for urological care. Aspiration and irrigation of the corpora cavernosa was proposed, but could not be performed because of patient refusal, and the erection resolved spontaneously after 10 hours. Haloperidol was stopped, and four days later the patient was switched to 10mg per day of olanzapine. After 10 days of treatment, he developed a second episode of priapism, and olanzapine was also stopped. A cavernosal aspiration-irrigation was performed in emergency; which resulted in the partial detumescence of the penis. Two days later, and despite therapeutic abstention, the patient presented another episode of priapism. The indication of a revascularization of the corpora cavernosa was proposed, but again the patient refused the surgery. Finally, the patient was administered 400mg/day of amisulpride, with a favorable outcome. Priapism disappeared after a month with the installation of fibrosis and partial loss of erectile function. DISCUSSION: The precise mechanisms of the role of AP in the occurrence of priapism are not all known and a multifactor etiology seems the most likely. Neuromuscular hypothesis is the most mentioned, involving the blocking action of alpha1-adrenergic receptors of the corpora cavernosa for which most of AP have an affinity. The occurrence of priapism in a psychotic patient, especially during periods of decompensation, raises a number of challenges for the medical staff. First, the non-recognition by the patient of this side effect, and its potentially severe consequences. Second, the absence of link between dose and duration of AP treatment on one side, and the onset of priapism on the other, which makes it hard to predict. The third challenge is the choice and initiation of another AP. The literature reveals many cases of priapism in both conventional and atypical AP, the presence of a predisposition to this type of incident has been reported. However, few authors have focused on alternatives to provide for these patients. Amisulpride is currently the only molecule that does not have alpha-adrenergic affinity and is therefore preferred in these cases. CONCLUSION: Priapism is a rare but serious adverse event of AP medication. Informing patient about the risk of priapism would help to report it early and prevent erectile dysfunction. Switching to another AP with less alpha1-blocking properties is generally recommended.

[Neuropsychiatric symptoms revealing pseudohypoparathyroidism with Fahr's syndrome]. / Manifestations neuropsychiatriques révélant une pseudohypoparathyroïdie avec un syndrome de Fahr.

UNLABELLED: Fahr's syndrome is characterized by the presence of intracerebral, bilateral and symmetrical non-arteriosclerotic calcifications, located in the central grey nuclei. One of its main etiologies is pseudohypoparathyroidism (PHP), due to a resistance to the action of parathormone (PTH) with essentially hypocalcaemia and a normal or a high rate of PTH. CASE REPORT: Mr B.A. is a 36-year-old man, admitted to hospital because of refractory psychotic symptoms associated with alcohol abuse and fits of convulsion, for diagnostic and therapeutic update. Mr B.A. had presented convulsions since the age of 10, without regular medical treatment. He showed a decrease in his school performances and started using alcohol. Since the age of 17, he began expressing delusions of persecution and of enchantment fed by the persistence of the convulsions. He was administered phenobarbital, and classic antipsychotics (haloperidol and levomepromazine) and developed serious extrapyramidal side effects, treated with an anticholinergic (trihexyphenidyl). Evolution was rather disadvantageous: more epileptic fits, exaggeration of tremors; abuse of alcohol and persistence of psychotic symptoms. On admission, psychiatric examination objectified paranoid delusions of being possessed and persecuted by others. Neurological examination revealed the presence of limb tremors, with a positive Froment's sign on the right, and dysarthria. Other than this, the patient was shorter in comparison with his siblings and exhibited bad dentition. A CT brain scan found bilateral, symmetric basal ganglia calcifications, confirmed by MRI, in favour of Fahr's syndrome. Phosphocalcic investigations revealed a low concentration of serum calcium (65 mg/l) and a hyperphosphataemia (60.1mg/l). The blood level of parathyroid hormone was in the upper limit of normal (66 ng/l), and levels of thyroid hormones and thyroid-stimulating hormone were normal. The diagnosis of Fahr's syndrome, revealing a pseudohypoparathyroidism was posed, and the patient was orientated to endocrinology after readjustment in his therapy (sodium valproate and olanzapine). DISCUSSION: About 40% of the patients with Fahr's syndrome are seen with primarily cognitive and other psychiatric findings. For this patient, hypocalcaemia was at the origin of his convulsions, and the use of phenobarbital, known for its hypocalcemiant action, provoked the inverse result. Alcohol drinking also aggravated hypocalcaemia, and maintained the fits. The use of classic antipsychotics and anticholinergic agents, amplified the extrapyramidal signs caused by Fahr's syndrome. Recognizing the origin of the symptoms allowed rethinking the therapeutic strategy according to all these elements. CONCLUSION: Psychiatrists should consider Fahr's syndrome as a differential diagnosis in the evaluation of psychosis associated with convulsions. This case, along with others in the literature, further emphasizes the importance of the role of neuro-imaging and the search for disrupted phosphocalcic metabolism in patients with atypical or refractory psychotic symptoms.