Nisaharan Srikandarajah

Does early surgical decompression in cauda equina syndrome improve bladder outcome

Study Design. We analyzed retrospectively whether early surgery for cauda equina syndrome (CES) within 24, 48, or 72 hours of onset of autonomic symptoms made any difference to bladder function at initial outpatient follow-up. Objective. CES potentially causes loss of autonomic control including bladder dysfunction, resulting in significant disability. There is significant debate regarding appropriate timing of surgery. Summary of Background Data and Methods. We conducted a retrospective cohort study of 200 patients between 2000 and 2011 who underwent decompressive surgery for CES at a regional neurosurgical center. Data collected were from clinical admission and at initial follow-up. Presentation was categorized into CES with retention (CESR) and incomplete CES (CESI) and duration of autonomic symptoms before surgical intervention. Results. A total of 200 patients had complete clinical records; 61 cases with CESR and 139 cases with CESI. Average initial follow-up time was 96 days. For the 36 cases with CESI less than 24 hours, normal bladder function was seen at follow-up in all patients except 4 (11.1%), but with 103 cases with CESI more than 24 hours, 48 (46.6%) had bladder dysfunction (Pearson &khgr;2P = 0.000). For the 64 cases with CESI less than 48 hours, normal bladder function was seen at follow-up in all except 10 (15.6%), but with 75 cases with CESI more than 48 hours, 42 (56%) had bladder dysfunction (Pearson &khgr;2P = 0.000). For the 35 patients with CESR, operating within 24, 48, or 72 hours made no obvious difference to bladder outcome. Data were also reanalyzed changing the dataset groups to CESI less than 24 hours, 24 to 48 hours, and more than 48 hours to calculate odds ratios regarding normal bladder outcome. Conclusion. We identified that decompressive surgery within 24 hours of onset of autonomic symptoms in CESI reduces bladder dysfunction at initial follow-up, but no statistically significant difference in outcome was observed in CESR regarding timing of operation. Level of Evidence: 3

Indications for intracranial reservoirs: A six-year study

Abstract Objectives. For patients with intracranial recurrent cysts, reservoir placement can offer symptomatic control at relatively low risk, allowing repeated outpatient aspiration. Predicting which patients will require repeated drainage is not always straightforward. The aim of this study was to examine a series of patients treated with reservoir system placement, and examine the factors that may be relevant to repeated drainage and morbidity. Methods. We retrospectively reviewed all adult patients who had intracranial reservoir placement between 2005 and 2011 at a single neurosurgical centre. Information was gathered on the indications for placement, demographics, diagnosis, imaging, disease characteristics, complications and clinical outcome. Results. Forty-one adult patients had reservoir placement over the 6-year period, of which 31 had cystic lesions, 4 had hydrocephalus, and 6 were for intrathecal therapy. Of the 31 cystic lesions, 14 were high-grade gliomas, 6 craniopharyngiomas, 4 low-grade gliomas, 5 cystic metastases, 1 acoustic neuroma, and 1 arachnoid cyst. The 30 patients with malignant disease had 1–6 postoperative aspirations at a median of 290 days after surgery. In patients with hydrocephalus the reservoir was not used postoperatively. Eighty-three per cent of patients with cystic lesions who had recurrent aspirations (26/36) resulted in clinical improvement. For the three categories of cystic lesions with the most number of aspirations; 100% showed clinical improvement in low-grade lesions, 68.4% in high-grade lesions, and 66.7% in craniopharyngiomas. Four patients experienced complications, including reservoir malfunction (2), infection (1), and misplacement (1). Conclusions. Intracranial reservoirs provide significant clinical improvement when used for recurrent aspiration in patients with cystic tumours. In particular, it is clear that ommaya reservoirs are of significant advantage in high-grade lesions, where the majority of patients undergo recurrent aspirations with clinical improvement.

Serial imaging and management of ganglioglioma with unusual presentation and meningeal spread

Dear Editor, We report the case of a 28-year-old female with migrainous headaches and refractory epilepsy from a ganglioglioma with leptomeningeal extension treated with serial imaging, stepwise medical management, and surgical resection. Gangliogliomas are rare intra-axial tumors (around 1% of cranial CNS neoplasms) of mixed neuronal and glial origin that most commonly occur in the temporal lobes and present with refractory epilepsy predominantly in children and young adults [3, 7]. She described 20 months of a constant left fronto-temporal headache with daily throbbing exacerbations, aggravated by movement, sound, and light. She had no neurological deficits and an ECOG (Eastern Cooperative Oncology Group) score of 1. Her past medical history included depression. Her family history included brain tumors, depression, breast and cervical cancer, but no epilepsy. She developed intermittent diplopia without any obvious ocular cause, 6 weeks of weight loss, and reduced appetite. Moderate pleocytosis on CSF analysis suggested chronic inflammation. MR imaging showed left hippocampal head expansion with T2 hyperintensity and T1 hypointensity. The left postero-lateral midbrain, superior left cerebellar hemisphere cortex and the vermis with its adjacent white matter on the right showed T2 hyperintensity. Contrast demonstrated a homogenously enhancing ovoid lesion arising from the left hippocampal head, extending into the left lateral ventricle temporal horn. Florid thick dural and leptomeningeal enhancement along the left cerebellar convexity, right side of the vermis, left temporal lobe convexity, postero-lateral midbrain, and anterior pons (with enhancement along the left trigeminal nerve) was present. Certain areas suggested intraaxial extension. Enhancing nodules were identified at the right lateral ventricle anterior pole and along the right side of the anterior falx. Figure 1 shows representative images. Her gallium scan was normal. Biopsy in December 2009 was compatible with a low-grade glioma, and possibly a ganglioglioma. Her MRI in July 2010 was unchanged. Biopsy of the meningeal enhancement to exclude a second pathology was considered too hazardous given her symptoms. Despite reporting worsening memory in March 2011, neuropsychological assessment found her cognitive functioning to be average or better in all domains tested, but identified signs of severe anxiety and moderate depression. Nearly 2 years post presentation, partial and generalized tonic clonic seizures developed. Lamotrigine was commenced in May 2012, increasing to 50 mg BD. After MR imaging demonstrated lesion growth, it was excised in October 2012. The histology showed a biphasic tumor composed of ganglioid cells demonstrating a large amphophilic cytoplasm containing vesicular nuclei with prominent nucleoli and * Andrew Dapaah andrewdapaah@silver-rain.com

Eyelid apraxia associated with deep brain stimulation of the periaqueductal gray area

We report a patient with eyelid apraxia following deep brain stimulation of the periaqueductal gray area. Based on the position of our electrode, we argue that the phenomenon is linked to inhibition of the nearby central caudal nucleus of the oculomotor nucleus by high frequency stimulation.

Letter to the editor of Acta Neurochirurgica: transient splenial lesion in a pre-surgical epilepsy patient – a no-touch lesion

Dear Editor, We would like to report the finding of a transient splenial lesion in an epilepsy patient undergoing pre-surgical work-up for a lesion in the left parahippocampal gyrus. There is documentation in the literature of clinically silent lesions in the splenium of the corpus callosum in patients with epilepsy. The aetiology and pathogenesis is largely unknown [2, 7, 8]. These lesions usually do not cause neurological deficits and disappear after weeks to months. It is a recognized phenomenon within neuroradiology, recently abbreviated to RESLES (reversible splenial lesion syndrome) [2], however not widely in neurosurgical literature, particularly in the presence of another known presumed neoplastic lesion. A 19-year-old left-handed female student was discussed at the Epilepsy Surgery meeting. She had a 9-year history of drug-resistant, complex partial seizures. Seizure frequency was one to two stereotypical automatisms per week after she was changed to lamotrigine 200 mg BD. The patient has no additional significant history. On examination, she was GCS 15 with no focal neurology, and neuro-cognitive examinations were unremarkable. Her initial imaging in early 2010 showed a left posterior parahippocampal gyrus abnormality. Considering the clinical scenario and the radiological appearances, the likely differentials were a low-grade glioma or dysembryoplastic neuroepithelial tumour. Follow-up imaging showed no interval change of the left hippocampal lesion, but there was an ovoid area of increased signal (on T2W images) within the splenium of the corpus callosummeasuring 12mm by 7.5 mm axially (Fig. 1), which was not present on the previous studies. It demonstrated restricted diffusion and did not enhance. Functional MRI demonstrated left hemisphere language dominance with primary language centres distant from the left hippocampal lesion. Video telemetry in November 2012 captured two typical seizures associated with rhythmic slow activity over the left cerebral hemisphere. Her EEG in January 2013 was within normal limits. The patient’s routine blood results were all within normal range, and she did not exhibit any clinical signs of lamotrigine toxicity. As a result, no change was made to her medication, and repeat MRI imaging seven months later in March 2013 showed complete resolution of the corpus callosum lesion (Fig. 1). Clinically silent, transient lesions of the corpus callosum due to seizure activity, AED toxicity, and cerebral infections where AED treatment is not involved have been described in the literature [2, 9]. Differentials of such lesions based on imaging alone include ischaemia, posterior reversible encephalopathy syndrome, multiple sclerosis, Marchiafava–Bignami disease, diffuse axonal injury, and extrapontine myelinosis. Most AEDs have been implicated in the cause of these lesions [1, 3–8]. There does not seem to be a predilection for age, sex, AED treatment, or seizure type in causing these lesions. This suggests the possibility of different processes leading to one common causal pathway. The frequency of reversible splenial lesions in patients who undergo pre-op evaluation for epilepsy surgery lies at less than 1 % [5]. Polster et al., 2001 [7] suggested rapid AED change or even transient arginine-vasopressin imbalance due to AED withdrawal as possible etiologies. Gurtler et al., 2005 [3] compared 16 patients with a splenial lesion to 32 control patients and found no difference in the frequency of seizures N. Srikandarajah : J. O. Farah Department of Neurosurgery, The Walton Centre, Liverpool, UK