Models of Traumatic Cerebellar Injury

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. Animal models of TBI have begun to explore the vulnerability of the cerebellum. In this paper, we review the clinical presentation, pathogenesis, and putative mechanisms underlying cerebellar damage with an emphasis on experimental models that have been used to further elucidate this poorly understood but important aspect of TBI. Animal models of indirect (supratentorial) trauma to the cerebellum, including fluid percussion, controlled cortical impact, weight drop impact acceleration, and rotational acceleration injuries, are considered. In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective

Use of sildenafil in the treatment of erectile dysfunction in patients with spinal cord injury

Erectile dysfunction (ED) is one of the major complications after spinal cord injury (SCI) that decreases the quality of life of the patients. Although many efforts have been made to decrease ED, they are frequently cumbersome, with a high failure rate. The aim of this study was to assess the effects of sildenafil citrate at several doses, an oral agent that has been shown to improve a broad spectrum of ED. Sixty male patients with SCI were divided into 2 groups and received 25 mg or 50 mg sildenafil citrate, respectively, during a 4-week treatment period I hour before sexual intercourse. Our results demonstrated that sildenafil citrate significantly improved reflexogenic erectile response in both groups (P = 0.02 and P = 0.01, respectively). Subjects receiving sildenafil citrate reported that treatment had significantly improved their erections, frequency of sexual intercourse, satisfaction, enjoyment, sexual desire, overall sex life, sexual relationship, and self-confidence in erections (P 0.05). The authors concluded that sildenafil citrate might be used effectively for the treatment of ED in patients with SCI, even in a low-dose (25 mg) regimen

Spontaneous intracranial hypotension after labor without spinal intervention

We present a 29-year-old woman admitted with severe postural headache after spontaneous term labor. Lactation ceased for the duration of headache. Magnetic resonance imaging (MRI) revealed dural thickening that is suggestive of spontaneous intracranial hypotension. CT-cisternography disclosed cervicodorsal dural leak. She was treated with a high-volume epidural blood patch (EBP) and her symptoms were relieved. Lactation returned to normal after EBP. She had normal findings on follow-up MRI examination at 6 months

Surgical treatment of intracranial epidermoid tumors

Intracranial epidermoid tumors are rare, potentially curable, benign lesions that are sometimes associated with perioperative complications, and tend to recur if not completely removed. Histologically benign epidermoid tumors may also develop into highly malignant tumors. This study evaluated on 28 cases of intracranial epidermoid tumor treated over a 13-year period by radical resection with micro-neurosurgical techniques. The majority of patients underwent computed tomography and/or magnetic resonance imaging within the first 24 hours postoperatively to confirm the results of surgery. Radical surgical resection was achieved in 21 of the 28 cases, and there was no operative mortality. The most common postoperative complication was transient paresis of various cranial nerves. During a mean follow up of 6 years, only one tumor became malignant. Radical surgical resection should be the goal in treating these benign lesions, but if not possible, every effort should be made to minimize the amount of tumor tissue that remains

Two cases of neuro-Behçet's disease mimicking cerebral tumor

Two cases of neuro-Behçet's disease with isolated, solitary fronto-temporal and mesencephalic lesions respectively are reported. The cases were misdiagnosed as cerebral tumor. The postoperative outcome of the first patient was not satisfactory as he developed hemispheric edema. The second patient, with mesencephalic lesion, was treated only with corticosteroids, and the patient improved significantly. The lesion in this case resolved completely at six-month follow-up. We conclude that distinguishing the isolated solitary cerebral lesion of the Behçet's disease from a tumor may prevent surgical intervention

Concentrations of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) in cerebrospinal of patients with severe head injuries

There is growing evidence that nitric oxide (NO) produced by isoforms of nitric oxide synthase (NOS), namely, inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS), plays a role in neuronal damage after neurotrauma. NO is a powerful universal mediator of many biologic reactions, including the mechanisms of injury during head trauma. Understanding of the organization and function of NO and NOS has led to new concepts in the treatment modalities of neuronal damage after head injury. In the current study, nine consecutive patients with a severe head injury who were admitted to Cerrahpasa Medical School Hospital at the University of Istanbul between January 2001 and July 2001 were evaluated. Cerebrospinal fluid (CSF) samples were withdrawn from the intraventricular catheter at admission (4-8 hours after trauma) and on each of the next 3 days. The iNOS and nNOS concentrations were assayed in 72 samples of ventricular CSF. CSF concentrations of iNOS and nNOS were increased after severe closed-head injury and peaked at 64 to 72 hours and 20 to 24 hours after trauma, respectively. These results suggest that maximal neuronal damage may occur between 20 and 24 hours after injury as a result of increased nNOS activity, which may contribute to the concomitant excitotoxic neuronal death after traumatic brain injury

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury

Study Design: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated