To investigate whether nestin would be a useful marker for retinal injury and also to ascertain a better understanding of the roles of Müller cells in the injured retina by the use of damaged rat retina.

A total of 33 adult female Wistar rats were used in this study. Three were used as controls and the remaining as retinal injury modes (6 for hypoxia; 15 for experimental glaucoma and 9 for optic nerve transection). Double immunofluorescence labeling was carried out between nestin and glutamine synthetase (GS), and between glial fibrillary acidic protein (GFAP) and GS antisera in normal and pathological retinae.

The results showed that there were no nestin nor GFAP staining in mature Müller cells of the normal retina. A major finding was that nestin expression was induced in Müller cells subjected to hypoxia, glaucoma and optic nerve transection.

These results suggest that nestin as well as GFAP (even more sensitive than GFAP) are useful and reliable biomarkers for retinal damage. The more intense expression of nestin, GFAP and GS in the end-feet of Müller cells suggest that they may help to maintain the retinal structural integrity and to enhance functional recovery in various retinal diseases.

Two prospective studies in patient with brain tumours were performed comparing the Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA). The first assessed their feasibility and the second compared their diagnostic accuracy against a four-hour neuropsychological assessment (NPA). The introduction of the NPA decreased accrual and retention rates. We were therefore concerned regarding potential selection bias.

Ninety-two patients were prospectively accrued and subsequently divided into three categories: a) no NPA required b) withdrew consent to NPA c) completed NPA. In order to quantify any potential bias introduced by the NPA, patient demographics and cognitive test scores were compared between the three groups.

There were significant differences in age (p<0.001), education (p=0.034), dexamethasone use (p=0.002), MMSE (p=0.005), and MoCA scores (p<0.001) across the different study groups. Furthermore, with increasing involvement of the NPA, patients' cognitive scores and educational status increased, while their age, dexamethasone use, and opioid use all decreased. Individuals who completed the NPA had higher MoCA scores than individuals who were not asked to complete the NPA (24.7 vs. 20.5; p < 0.001). In addition, this relationship held when restricting the analyses to individuals with brain metastases (p < 0.001).

In this study, the lengthy NPA chosen introduced a statistically and clinically significant source of selection bias. These results highlight the importance of selecting brief and well tolerated assessments when possible. However, researchers are challenged by weighing the improved selection bias associated with brief assessments at the cost of reduced diagnostic accuracy.

The etiology of complex regional pain syndrome (CRPS) is unknown. Different environmental and genetic factors have been postulated to contribute to CRPS.

We reviewed the clinical data from a cohort of 69 patients with CRPS. Four families were identified with two or more members affected with CRPS yielding a total of nine patients. Six more patients reported the presence of pain symptoms in their family members, however; this could not be clinically confirmed.

The case histories of the nine individuals with ‘familial’ CRPS suggested a younger age at onset and more frequent history of migraine versus the non-familial patients. A pattern of inheritance could not be ascertained.

This data supports the hypothesis that CRPS can be familial and hence may have a genetic basis in some families. Larger studies will be needed to ascertain clearer patterns of inheritance and to determine whether the clinical features of ‘familial’ CRPS are the same as the sporadic form.

Post-operative cerebrospinal fluid (CSF) leaks are a common complication of endoscopic pituitary surgery and account for a significant proportion of hospital costs associated with this procedure. Tisseel® is a tissue glue commonly used as an adjunct in dural repair but is not optimal for this purpose. DuraSeal® has several properties advantageous for dural repair but is not widely accepted in Canada partly due to its increased cost.

A cost analysis of DuraSeal® versus Tisseel® in endoscopic pituitary surgery.

A cost analysis was performed based on typical endoscopic pituitary surgery cases performed at our tertiary care institution. Operating room, hospital admission, and surgical sealant costs were obtained directly while estimates of patient recovery time and post-operative CSF leak rates were based on consensus values reported in the literature. Outcomes were reported for various possible clinical scenarios of sealant use.

In a model where surgical sealant is employed only in high-risk cases, use of DuraSeal® allows for a yearly cost savings of at least $4486.72. If surgical sealant is used in all cases, regular use of DuraSeal® versus Tisseel® either marginally reduces yearly costs or increases them by a maximum of $7619.25, depending on the case volume and estimated post-operative CSF leak rate.

In most clinical scenarios, use of DuraSeal® in endoscopic pituitary surgery may reduce overall yearly hospital costs compared to Tisseel®.

To ensure the overall quality of our electroencephalogram (EEG) laboratory, we decided to perform an audit of EEGs interpreted at our institution, focusing initially on EEGs reporting temporal abnormalities.

Reports of all EEGs performed between January 1st and June 30th, 2006 were reviewed in order to identify tracings mentioning abnormalities in the temporal regions. These records were then independently reviewed by two epileptologists on two distinct occasions, separated by an interval of at least six months. If the recording was considered normal after this process, the cause for misinterpretation was identified and the patient's chart was reviewed to determine if he was epileptic or not based on available evidence until June 2009.

In the first half of 2006,143 out of 773 EEGs mentioned temporal abnormalities (18.5%). In general, intra- and interrater agreement ratios between our two epileptologists were moderate to substantial for normality, presence of epileptic activity and presence of slowing. Forty-five recordings (31.5%) were reported as normal independently by them on two distinct sittings six months apart. The most common causes for misinterpretation were the presence of benign epileptiform variants, normal sharply contoured patterns of somnolence or hyperventilation. Chart review confirmed that most were non-epileptic patients (60% non-epileptic, 27% epileptic, 13% unknown).

Moderate to substantial intra- and interrater agreement as well as frequent misinterpretation of physiological variants indicate that some corrective measures need to be implemented to improve the consistency of EEG interpretation amongst our group of electroencephalographers.

Epileptiform electroencephalogram (EEG) asymmetries are not uncommon in juvenile myoclonic epilepsy (JME) and can contribute to the misdiagnosis of this syndrome. The objective of this study is to further characterize patients with focal or asymmetric epileptiform electroencephalographic abnormalities and more specifically in terms of response to treatment. Controversial data exists in the literature concerning this issue.

We retrospectively reviewed clinical and EEG data of a group of consecutive JME patients followed at our Epilepsy Service. The first EEG available for each patient was reviewed blindly by two independent electroencephalographers.

Twenty-eight patients with JME were identified: 11 (39.3%) were resistant to at least one appropriate anti-epileptic drug (AED), including valproate, lamotrigine, topiramate or levetiracetam. All patients except two had generalized epileptiform abnormalities. Overall, EEG asymmetries were detected in 57.1% of the cases. The proportion of EEG asymmetries between AED-sensitive group (52.9%) and AED-resistant group (63.5%) did not reach statistical significance. Concordance between examiners for identification of EEG asymmetries was good. Analysis of patients with and without asymmetries showed no statistically significant differences in comparisons of age, family history of seizure, presence of polyspike and slow wave, photosensitivity and timing of EEG related to the onset of treatment.

Asymmetric electroencephalographic abnormalities are frequent in patients with JME. These features should not be misinterpreted as being indicative of partial epilepsy. In our group, asymmetries were not associated with resistance to treatment.

To determine the correlation between frontal intermittent rhythmic delta activity (FIRDA) and the clinical and radiological correlates in children.

Retrospective review of the EEG and imaging studies of 37 children with documented FIRDA.

FIRDA was associated with multiple neurological conditions and not necessarily with midline lesions. Patients with abnormal neurological exam had a longer FIRDA duration (average 9.5 seconds) compared to children with no reported abnormal examination (average of 6.5 seconds). FIRDA ranged from 2 to 2.5 Hz (n=15), 3 Hz (n=17) and from 1.5 to 3 Hz (n=5) and there was a significant association between the duration of FIRDA and abnormal laboratory tests (p. < 0.05, Student's T test).

FIRDA was not correlated with midline brain lesions in children. FIRDA may be a non specific oscillation of an unhealthy pediatric brain with or without seizures.

Most studies of third nerve palsy (TNP) antedate computerized imaging and focus primarily on chart review of referral outpatients.

To compare a large contrasting population, I reviewed 1400 personally-examined municipal hospital inpatients with TNPs seen over 37 years.

TNPs were bilateral in 11%, complete in 33%, without other neurological signs (isolated) in 36%, and associated with recurrent cranial neuropathies in 7%. Third nerve damage occurred in the subarachnoid space in 32%, the cavernous sinus in 23%, the brainstem in 14%, as a nonlocalized peripheral neuropathy in 18% and at an uncertain location in 13%. Causes were trauma (26%), tumor (12%), diabetes (11%), aneurysm (10%), surgery (10%), stroke (8%), infection (5%), Guillain-Barre and Fisher syndromes (5%), idiopathic cavernous sinusitis (3%), benign self-limited (2%), miscellaneous (4%), and unknown (3%). Local causes, besides an abundance of trauma, included six cases involving cysticercosis, four with wound botulism, and one with coccidiomycotic meningitis. Of 234 patients with diabetes, microvascular ischemia was the cause of TNP in only two-thirds (five had aneurysms) and 53% of those with diabetic microvascular ischemia had pupillary involvement—often bilateral, suggesting concomitant autonomic neuropathy. Only 2% of aneurysms spared the pupil. Apainful onset occurred with 94% of aneurysm and 69% of diabetic cases.

Bilateral TNPs, multiple cranial neuropathies, and accompanying neurological signs were common among our inpatients, as were causes rare in outpatient settings such as severe trauma, transtentorial herniation, midbrain strokes, and the Guillain-Barre syndrome. Few cases remained undiagnosed and nondiabetic ischemia was rare.

Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS.

We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm.

Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients.

We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.