[Obesity isn't always obesity: Cushing's disease - case report]. / Offita er ekki alltaf offita: Cushing-sjúkdómur, sjúkratilfelli

Woman in her thirties presented to the emergency room with a two-week history of worsening headache and diplopia. For eight years she had suffered from progressive weight gain, diabetes and hypertension that didn't improve with lifestyle modification. A lumbar puncture demonstrated increased intracranial pressure and MRI a pituitary adenoma. Physical examination was consistent with Cushing's syndrome and endocrine workup confirmed Cushing's disease. Treatment was complex, including unsuccessful pituitary surgery and gamma knife radiosurgery, and eventually bilateral adrenalectomy with subsequent development of Nelsons syndrome. This case illustrates the diagnostic delay that many patients with CD suffer from.

[Occlusion of the vertebrobasilar artery. Case presentation and literature review]. / Lokun í botn- og hryggslagæð heila. Sjúkratilfelli og yfirlit

This paper is a case report of a 22 year old, previously healthy woman that presented comatose to the Emergency Room at Landspitali University Hospital Iceland. A CT image of the head on admission revealed a large right cerebellar infarct with oedema compressing the fourth ventricle. A CT angiogram on admission was suspicious for a dissection of the left vertebral artery (confirmed during endovascular treatment) and a total occlusion of the distal third of the basilar artery. Thrombolytic therapy with t-PA was initiated followed by thrombectomy with good recanalization. The following day the patient underwent suboccipital craniotomy for malignant cerebellar infarction. She made a good clinical recovery to a modified Ranking scale of 1 at 90 days after discharge from the hospital. Following the case is a literature review on the clinical aspects of occlusion of the vertebrobasilar system, use and utility of imaging and treatment with (anticoagulation, IV and IA thrombolysis) modalities that have been tried. Finally, the evidence regarding thrombectomy and the role of craniotomy for malignant stroke are reviewed.

Hypopituitarism 3 and 12 months after traumatic brain injury and subarachnoid haemorrhage.

OBJECTIVE: High prevalence of hypopituitarism (HP) has been reported after traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH). The aim of the study was to prospectively evaluate the prevalence and progression of HP in patients after TBI and SAH in Icelandic population. DESIGN: A 12 month prospective single-centre study. METHODS AND PROCEDURES: A total of 27 patients were included, 15 patients with TBI and 12 patients with SAH. Pituitary function was evaluated with baseline hormone measurements and diagnostic tests. An insulin tolerance test was used unless contraindicated, then the GHRH-arginine test and Synachten test were used. RESULTS: At three months, 16.7% (2/12) of the patients had HP after TBI and 33.3% (4/12) after SAH. At 12 months, 21.4% (3/14) of patients had HP after TBI and 9.1% (1/11) after SAH. Gonadotropin deficiency was the most common deficiency at 3 months and GH and gonadotropin deficiency at 12 months. CONCLUSIONS: There is a considerable risk of HP after TBI and reason to study pituitary function further in patients with SAH. We believe that neuroendocrine evaluation is important in these patients. Since recovery commonly occurs 12 months after the event, evaluation should be performed after that time if not clinically indicated earlier.

Thyrotoxicosis in a 13-year-old girl following pituitary adenectomy for Cushing's disease.

Our objective is to report a case of thyrotoxicosis following pituitary adenectomy for Cushing's disease, the only pediatric case to our knowledge. No thyroid antibodies were detected, and the thyrotoxicosis was successfully treated for 3 months with no relapse after 5 years of follow-up. The cause of thyrotoxicosis remains unknown.

Extramedullary Cavernous Hemangioma with Intradural and Extradural Growth and Clinical Symptoms of Brown-Séquard Syndrome: Case Report and Review of the Literature.

BACKGROUND: Primary spinal tumors are rare. Symptoms depend on the size and location of the tumor. CASE DESCRIPTION: A patient presented with a rare clinical finding, Brown-Séquard syndrome. The symptoms were caused by an extramedullary tumor compressing on the thoracic spinal cord. Pathologic examination showed cavernous hemangioma with growth both intradurally and extradurally. CONCLUSIONS: This is an extremely rare finding; to our knowledge, only 1 case report has been published before in which a spinal cavernous hemangioma had intradural and extradural growth. The clinical symptoms of Brown-Séquard syndrome have not been described before in the findings of spinal cavernous hemangiomas.

[Superior canal dehiscence - Case report].

UNLABELLED: Superior canal dehiscence is a rare syndrome. The symptoms consist of hearing loss, dizziness and autophonia. The patient can be cured with surgery. A 28 year old woman went to several doctors for several months due to diminished hearing, dizziness and autophonia. The symptoms got worse. A work-up led to the diagnosis of superior canal dehiscence in the left ear. She underwent surgery and her symptoms improved. A latency in diagnosis is expected as the syndrome is rare. It's important to think of superior canal dehiscence when patients complain of these symptoms. KEY WORDS: superior canal dehiscence, autophonia, dizziness, hearing deficit. Correspondence: Bryndis Baldvinsdottir, bryndisbaldvins@gmail.com.

Secondary insults following traumatic brain injury enhance complement activation in the human brain and release of the tissue damage marker S100B.

OBJECT: Complement activation has been suggested to play a role in the development of secondary injuries following traumatic brain injury (TBI). The present study was initiated in order to analyze complement activation in relation to the primary brain injury and to secondary insults, frequently occurring following TBI. METHODS: Twenty patients suffering from severe TBI (Glasgow coma score ≤ 8) were included in the study. The "membrane attack complex," C5b9, which is the cytolytic end product of the complement system was analyzed in cerebrospinal fluid (CSF). The degree of brain tissue damage was assessed using the release of S100B and neuron-specific enolase (NSE) to the CSF and blood. The blood-brain barrier was assessed using the CSF/serum quotient of albumin (Q (A)). RESULTS: Following impact, initial peaks (0-48 h) of C5b9, S100B, and NSE with a concomitant loss of integrity of the blood-brain barrier were observed. Secondary insults at the intensive care unit were monitored. Severe secondary insults were paralleled by a more pronounced complement activation (C5b9 in CSF) as well as increased levels of S100B (measured in CSF), but not with NSE. CONCLUSION: This human study indicates that complement activation in the brain is triggered not only by the impact of trauma per se but also by the amount of secondary insults that frequently occur at the scene of accident as well as during treatment in the neurointensive care unit. Complement activation and in particular the end product C5b9 may in turn contribute to additional secondary brain injuries by its membrane destructive properties.