Rathke's cleft cyst as a cause of growth hormone deficiency and micropenis

Rathke's cleft cyst has rarely been reported in pediatric patients, and such cysts are usually found by chance, in 2–33% of routine necropsies, as they have not interfered with pituitary function. In general, they are intrasellar with a single layer of ciliated cuboidal or columnar epithelium containing mucoid material. The age range in which symptomatic Rathke's cleft cysts occur is between 30 and 60 years. This paper reports an 8.1-year-old boy presenting with growth hormone deficiency and micropenis attributable to hypogonadotropic hypogonadism (HH), implying altered pituitary function since intrauterine life. At this age (before puberty) the diagnosis of HH can be made by means of the LHRH agonist stimulation test, since conventional LHRH is not able to discriminate HH from a normal prepubertal child. To our knowledge, this is the first case of micropenis caused by Rathke's cleft cyst interfering with gonadotropin and growth hormone secretion since intrauterine life. Received: 5 October 1998 Revised: 8 November 1998     

Arachnoid cyst associated with painful tic convulsif

Combined clinical presentation of hemifacial spasm and ipsilateral trigeminal neuralgia is known as painful tic convulsif (PTC). It is a rare condition and the most common cause is vascular compression. We report an arachnoid cyst of the posterior fossa that caused PTC in a 50-year-old woman. Her radiological evaluation revealed a median, well-circumscribed, cystic lesion of the posterior fossa suggestive of arachnoid cyst, pushing the cerebellum and brainstem anteriorly. Midline suboccipital craniotomy and marsupialization of cyst was performed with complete recovery of symptoms. To our knowledge, this is the first report of a retrocerebellar arachnoid cyst causing PTC.     

Arachnoid cyst with rupture into the subdural space.

Arachnoid cysts which develop in relation to the cerebral hemispheres are usually found in the middle cranial fossa. These cysts are usually asymptomatic but can produce symptoms if there is haemorrhage into the cyst or the development of an associated subdural hematoma. Recent publications have emphasised the association of arachnoid cysts of the middle fossa with subdural haematomas. This report describes a case of an asymptomatic arachnoid cyst which ruptured into the subdural space. This event was followed by the development of symptoms despite the lack of haemorrhage.     

Arachnoid cyst presenting as subdural hygroma.

Arachnoid cysts are developmental lesions which are usually asymptomatic or may present with a variety of clinical features. Subdural hygroma is an extremely unusual complication associated with arachnoid cysts. A case of subdural hygroma that developed after the rupture of an asymptomatic middle cranial fossa cyst, following minor head injury is reported.     

Arachnoid cyst in a patient with psychosis: Case report

Background  

The aetiology of a psychotic disturbance can be due to a functional or organic condition. Organic aetiologies are diverse and encompass organ failures, infections, nutritional deficiencies and space-occupying lesions. Arachnoid cysts are rare, benign space-occupying lesions formed by an arachnoid membrane containing cerebrospinal fluid (CSF). In most cases they are diagnosed by accident. Until recently, the coexistence of arachnoid cysts with psychiatric disturbances had not been closely covered in the literature. However, the appearance of some references that focus on a possible link between arachnoid cysts and psychotic symptoms has increased the interest in this subject and raised questions about the etiopathogeny and the therapeutic approach involved.     

Arachnoid cyst rupture with subdural hygroma: case report and literature review

Arachnoid cyst rupture causing subdural hygroma is rare. Twenty-one cases have been previously reported in the literature. We report a case of a 9-year-old boy presenting signs and symptoms of increased intracranial pressure due to the rupture of a type III arachnoid cyst causing subdural hygroma. The clinical and radiological findings as well as the management of the patient are discussed in relation to the pertinent literature.     

Chronic hydrocephalus associated with short stature and growth hormone deficiency

A 28-year-old man with chronic hydrocephalus due to aqueductal stenosis was found to have a subnormal response of growth hormone to arginine infusion. It is postulated that compression of the pituitary by the enlarged third ventricle produced a deficiency of growth hormone and short stature.     

儿童蛛网膜囊肿破裂致硬膜下积液1例病例报告及文献复习

目的:探讨儿童蛛网膜囊肿合并硬膜下积液的病因、临床特征及治疗方法。方法:报告1例儿童左颞蛛网膜囊肿破裂致硬膜下积液病例,结合文献探讨该疾病的病因、临床表现、影像学特征及治疗。结果:在蛛网膜囊肿破裂致硬膜下积液的病例中,80%病例的囊肿位于中颅窝,半数以上病例有明确外伤史,CT或MRI可明确诊断,治疗多采取引流或开窗手术。结论:蛛网膜囊肿和硬膜下积液相关联的病例少见。CT或MRI具有诊断价值,一般采取手术治疗,目前倾向引入显微手术及内窥镜技术来治疗,建议根据囊肿类型选取分流手术。     

Sleep disturbance in children with growth hormone deficiency.

We examined the effects of growth hormone (GH) deficiency on sleep development by performing all-night polysomnography in three female children with GH deficiency (GHD). The percentage of REM sleep seemed to be reduced before the treatment in 2 cases, and human GH (hGH) compensation slightly increased it. Submental twitch movements (mTMs), i.e., body movements during sleep localized in the submental muscle and lasting less than 0.5 seconds, were commonly disturbed in the three patients. Rapid eye movements in REM sleep (REMs) were reduced before the therapy in one case, this decrease being reversed on hGH compensation. REMs also seemed to increase after hGH treatment in the other two cases. Dopamines and cholinergic muscarinic agonists can cause GH release, while mTMs and REMs might be related to dopaminergic and cholinergic systems in the human brain. It is intriguing that GHD, and the disturbance of mTMs and REMs coexisted in children with GHD. Since a relatively poor social outcome in patients with GHD has been reported, even after hGH compensation, it is important to monitor their neurological development by means of evaluation of their sleep disturbance.     

Arachnoid cyst with intracystic haemorrhage and subdural haematoma: case report and literature review

Abstract Arachnoid cysts (AC) are usually asymptomatic. However, very rarely they can become symptomatic due to cyst enlargement or haemorrhage, often after head trauma. In such cases bleeding is often confined to the subdural space, but intracystic haemorrhage has rarely been observed. We report a case of a child who had intracranial hypertension syndrome due to a right middle cranial fossa AC with intracystic bleeding and subdural haematoma.     

Arachnoid cyst rupture with subdural hygroma: report of three cases and literature review

INTRODUCTION: Arachnoid cysts are believed to account for about 1% of all intracranial expansive lesions, some remain inactive throughout life, others lie dormant for many years before clinical manifestation. In a few cases, arachnoid cysts have ruptured after cranial trauma or more rarely, spontaneously, with resultant subdural haemorrhage or CSF collection. CASE REPORT: We report three cases with traumatic rupture of arachnoid cyst into the subdural space in children, which is an extremely unusual complication. DISCUSSION: A review of the literature revealed only 18 previously reported cases.     

Effects of growth hormone substitution on mental performance in adults with growth hormone deficiency: a pilot study

Five patients ages 22 to 36 years with growth hormone deficiency received substitution with native human growth hormone and biosynthetic methionyl human growth hormone, 8 IU i.m. three times weekly, for two separate 4-week periods. Before and at the end of each treatment period, five psychometric tests evaluating cognitive functions were performed. The results suggest a beneficial effect of growth hormone on certain cognitive functions. The results were similar for the two hGH preparations.     

Childhood-onset growth hormone deficiency, cognitive function and brain N-acetylaspartate

Cognitive deficits have been reported in adults with childhood-onset growth hormone (GH) deficiency. We evaluated cognitive deficits simultaneously with parameters for neuronal integrity using (1)H magnetic resonance spectroscopy (MRS) in a cross-sectional design. We studied 11 adults (mean age 24.5 years) with childhood-onset GH deficiency, which persisted after reaching final height. All subjects were evaluated after interruption of GH supplementation for at least 3 months. We performed neuropsychological assessment (NPA) using tests evaluating memory, mental processing speed, reading ability and executive functioning. MRS was used to assess brain N-acetylaspartate (NAA)/choline ratios. Data were compared with an age-, sex- and education-matched control group (n=9, mean age 27.3 years). NPA demonstrated attenuated performance of the patients in the delayed verbal memory recall score (P<0.05) and the trail making A test (P<0.05), a measure of planning of behavior, processing speed and attention. Other neuropsychological tests were not affected. NAA/choline ratios were significantly reduced (P<0.01) in GH deficient subjects. Specific cognitive defects indicating affected memory and attention were found in patients with childhood-onset GH deficiency. These defects occur simultaneously with reduced neuronal integrity.     

Arachnoid cyst associated with subdural hematoma: report of three cases and review of the literature

Introduction  Arachnoid cysts are usually found incidentally and are generally asymptomatic. They are thought to be developmental anomalies, and their etiology is unknown. Some complications such as subdural hematoma, subdural hygroma, and intracystic bleeding can occur after minor traumas. Case report  Here, we report three cases. Case 1 has subdural hematoma associated with subdural hygroma, case 2 has subdural hematoma after a birth delivery, and case 3 has intracystic bleeding associated with subdural hematoma. Discussion  We suggest to treat the complicating event in our patients and have chosen burr-hole evacuation for treatment.     

Arachnoid cyst of the cerebellopontine angle associated with gliosis of the eighth cranial nerve.

The clinical syndrome produced by a cyst in the cerebellopontine angle (CPA) may closely mimic that of an acoustic neuroma, with sensorineural hearing loss, impaired corneal reflex, and cerebellar signs with increased intracranial pressure. Facial palsy is seldom reported. Gliosis of the eighth nerve is common but its association with CPA arachnoid cyst is very rare and not previously reported. We report a patient with a CPA arachnoid cyst associated with gliosis of the eighth cranial nerve. He presented with right peripheral facial palsy, and gliosis of the eighth nerve was diagnosed intraoperatively. CPA arachnoid cysts should be included in the differential diagnosis of peripheral facial palsy and the eighth cranial nerve should be examined during the resection and fenestration of the arachnoid cyst.     

Night sleep EEG and daytime sleep propensity in adult hypopituitary patients with growth hormone deficiency before and after six months of growth hormone replacement

BACKGROUND: Hypopituitary patients with growth hormone deficiency (GHD) complain of reduced vitality, general fatigue, lack of concentration, irritability and reduced alertness during daytime. It is unclear whether these symptoms are primarily due to GH-deficiency and/or secondary to GHD related sleep impairments. Bi-directional interactions between the somatotropic system and human sleep patterns are well established. However, data on the effect of GH either in subjects without GHD or in patients with GHD under GH replacement therapy on the sleep electroencephalogram (EEG) are controversial. No reports exist about objective measures of daytime sleepiness in GH deficient patients before and during GH-therapy. OBJECTIVE: To assess the effects of GH on nocturnal and daytime sleep in adult patients with GHD before and during recombinant human GH (rhGH, Somatropin) replacement therapy. METHODS: Eighteen adult patients with GHD (4 women and 14 men) participated in the study. Mean age at the beginning of the study was 48.5 years (range 27-64 years). Ten patients were recruited from a double-blind, randomized placebo controlled trial over 6 months, followed by an open treatment period of 6 additional months (Group I). In all patients from this group, only the effects of the first 6 months of GH treatment were assessed. Eight additional patients were treated in an open study design for 6 months (Group II). Nocturnal sleep recordings and daytime sleep EEGs with a multiple sleep latency test were performed at baseline and after 6 months of additional GH replacement therapy. RESULTS: One patient dropped out due to side effects and was not included in sleep analysis. IGF-1 levels were increased in all patients, partially in a supraphysiologic range. Side effects were mainly mild but in one patient (from group II), general muscle pain led to interruption of the study. Therefore sleep analysis was only done in 17 patients. Sleep parameters were comparable to healthy control groups from the literature. GH substitution over 6 months did neither affect total sleep time nor times spent in different sleep stages. REM sleep density was also not changed. Daytime sleep propensity as measured by the multiple sleep latency test was not influenced by GH treatment. CONCLUSIONS: GH replacement does neither affect night sleep nor daytime sleep propensity in GH deficient hypopituitary adults. GH substitution has no sleep disturbing effect.