Huntington’s Disease Complicated by Traumatic Subarachnoid Bleeding and Subdural Hematoma

Though Huntington’s Disease (HD) is frequently complicated by falls and consecutive Traumatic Brain Injury (TBI) with Subdural Hematoma (SDH), traumatic Subarachnoid Bleeding (SAB) has not been reported as a complication of HD. A 67yo female with HD due to a CAG-repeat expansion of 43 repeats, diagnosed 18 months earlier, was admitted after a fall with a Glasgow-Coma Scale (GCS) score of 3. Cerebral CT on admission revealed bilateral SDH and SAB. No aneurysm could be detected on conventional angiography. After extubation, she was non-responsive to verbal requests and typical choreatic movement recurred. Tiaprid, olanzapine, and tetrabenazine were of limited effect. This case shows that falls in HD may not only cause SDH but rarely traumatic SAB. TBI in HD may worsen the phenotype and may increase the risk of a poor outcome.

Risk factors and treatment approach for subarachnoid hemorrhage in a patient with nine intracranial aneurysms

Introduction. In about one-third of the patients with aneurysmal subarachnoid bleeding, multiple intracranial aneurysms are confirmed. Risk factors such as female gender, smoking, hypertension, and age over 60 tend to be associated with multiple aneurysms. In this paper, we also discuss family predisposition and the treatment approach for multiple cerebral aneurysms. Case outline. Here, we present a case of a female patient, 64-year-old, with spontaneous subarachnoid hemorrhage that had nine intracranial aneurysms. The patient was treated for hypertension for a longer period, excessive smoker, and two of her nearest members of the family died from intracranial bleeding. The patient was fully conscious, without any neurological impairment. Subarachnoid bleeding was diffuse and nor brain-computer tomography finding nor digital subtraction angiography couldn't suggest the source or location of bleeding among nine presented aneurisms. Magnet resonance imaging had to be done, and the T1W fast spin-echo sequence showed a 9 mm large ruptured an aneurysm at the basilar tip, after contrast application, beside others. Three days after insult endovascular embolization was done and two basilar aneurysms were excluded from the circulation, including the one that bled. Conclusion. The patient had the majority of risk factors for multiple intracranial aneurysms. Knowledge of the family predisposition of multiple intracranial aneurysms allowed us to make proper diagnostics of a patient's descendant and reveal a new patient.

Acute subdural hematomas secondary to aneurysmal subarachnoid hemorrhage confer poor prognosis: a national perspective

BackgroundAneurysmal ruptures typically cause subarachnoid bleeding with intraparenchymal and intraventricular extension. However, rare instances of acute aneurysmal ruptures present with concomitant, non-traumatic subdural hemorrhage (SDH). We explored the incidence and difference in outcomes of SDH with aneurysmal subarachnoid hemorrhage (aSAH) as compared with aSAH alone.MethodsRetrospective cohort study from 2012 to 2015 from the National (Nationwide) Inpatient Sample (NIS) (20% stratified sample of all hospitals in the United States). NIS database (2012 to September 2015) queried to identify all patients presenting with aSAH. From this population, the patients with concomitant SDH were identified.ResultsA total of 10 075 patients with both cerebral aneurysms and aSAH were included. Of these, 335 cases of concomitant SDH and aSAH were identified. There was no significant change in the rate of SDH in aSAH over time. SDH with aSAH patients had a mortality of 24% compared with 12% (p=0.003) in the SAH only group, and only 16% were discharged home vs 37% (p=0.003) in the SAH group.ConclusionsThere is a 3.5% incidence of acute SDH in patients presenting with non-traumatic aSAH. Patients with SDH and aSAH have nearly double the mortality, higher rate of discharge to nursing home and rehabilitation, and a significantly lower rate of discharge to home and return to routine functioning. This information is useful in counseling and prognostication of patients with concomitant SDH and aSAH.

A Case Report of Cerebral Vasospasm Following Elective Clipping of Unruptured Aneurysm: Pathogenetic Theories and Clinical Features of a Dangerous Underestimated Event

Background and Importance: Angiographic-proven and clinically-evident cerebral vasospasm (CVS) after uneventful elective clipping of unruptured intracranial aneurysm (UIA) is a very rare and often underestimated event. To date, the knowledge of risk factors, pathophysiology, and demographic characteristics of these conditions are solely relegated to few case reports. With the aim of better characterize shared features and mechanism that could be involved in such event we also performed a review of the present literature and analyzed aneurysm’s features, surgical factors, treatments, recovery and of all reported cases of CVS after elective clipping. Clinical Presentation: We report a case of a cerebral vasospasm following elective clipping of a middle cerebral artery (MCA) bifurcation aneurysm in a 59-year-old woman who smoked next days after treatment, despite medical advice. We found ten cases comparable to ours with angiographic-proven and clinically evident cerebral vasospasm after uneventful elective clipping. Conclusion: Classic mechanisms of CVS following SAH have been widely studied. In all the cases we analyzed, no subarachnoid bleeding occurred, as demonstrated in pre and postoperative CT scans and intraoperatively. Various theories on the possible mechanism have been advanced. It seems reasonable that CVS following elective clipping of unruptured aneurysm is a multifactorial phenomenon. Although its pathogenesis is unclear, clinicians should keep in mind the existence of this event, that is rare, but it could be seen in the clinical practice of every neurosurgery ward. In our opinion, it’s worth to know this possible post-operative complication because, when suspected clinical signs and symptoms of delayed ischemic neurological deficit (DIND) arise after elective clipping, it’s important to make an early diagnosis of CVS owing to early treatments are critical to improve clinical outcome

Intralesional and subarachnoid bleeding of a spinal schwannoma presenting with acute cauda equina syndrome

We present an unusual case of spinal neurinoma with intralesional and subarachnoid bleeding with acute cauda equina syndrome. A 38-year-old man was admitted to our department after a minor thoracic spinal trauma with right lower limb plegia and urinary retention. MRI showed a T11 intradural tumour with intralesional and subarachnoid haemorrhage. The patient was operated of spinal cord decompression and complete tumour resection. The histological examination documented a schwannoma with large haemorrhagic intratumoural areas. A full neurological recovery was documented at 6-month follow-up.

Neurological Perspectives of Neurogenic Pulmonary Edema

Background: Neurogenic pulmonary edema (NPE) is characterized by acute respiratory distress triggered by acute, severe compromise of the central nervous system (CNS). This review aims at summarizing and discussing recent and previous findings about the type and frequency of CNS triggers of NPE, pathogenesis, diagnosis, treatment, and outcome of patients experiencing NPE. Key Messages: NPE is diagnosed in the presence of pink, frothy sputum, pulmonary edema, bilateral opacities on X-ray, PaO2:PiO2 <200 mm Hg, acute CNS compromise with increased intra-cranial pressure, rapid resolution within 48–72 h, and the absence of alternative causes of respiratory distress. The most common cerebral triggers of NPE include enterovirus-71-associated brainstem encephalitis, subarachnoid bleeding, intracerebral bleeding, traumatic brain injury, epilepsy, ischemic stroke, intracranial/spinal surgery, multiple sclerosis, electroconvulsive therapy, subdural/epidural hematoma, intoxication, hypoxia, and hydrocephalus. Simultaneous treatment of CNS and pulmonary compromise is required. Cerebral treatment involves infectiologists, neurologists, and neurosurgeons. Pulmonary treatment is mainly supportive, but if ineffective, extracorporeal membrane oxygenation or thermodilution are alternative options. Applying intensive care measures, the outcome of NPE has improved. Summary: CNS-disease triggering NPE is more variegated than anticipated. Delineation of NPE from other pulmonary or cardiac conditions mimicking NPE is crucial to take appropriate measures and improve the outcome of these patients.