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Cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL) is the most common monogenic form of small vessel disease characterized by migraine with aura, leukoaraiosis, strokes, and dementia. CADASIL mutations cause cerebrovascular dysfunction in both animal models and humans. Here, we showed that 2 different human CADASIL mutations (Notch3 R90C or R169C) worsen ischemic stroke outcomes in transgenic mice; this was explained by the higher blood flow threshold to maintain tissue viability compared with that in wild type (WT) mice. Both mutants developed larger infarcts and worse neurological deficits compared with WT mice, regardless of age or sex after filament middle cerebral artery occlusion. However, full-field laser speckle flowmetry during distal middle cerebral artery occlusion showed comparable perfusion deficits in mutants and their respective WT controls. Circle of Willis anatomy and pial collateralization also did not differ among the genotypes. In contrast, mutants had a higher cerebral blood flow threshold, below which infarction ensued, suggesting increased sensitivity of brain tissue to ischemia. Electrophysiological recordings revealed a 1.5- to 2-fold higher frequency of peri-infarct spreading depolarizations in CADASIL mutants. Higher extracellular [K.sup.+] elevations during spreading depolarizations in the mutants implicated a defect in extracellular [K.sup.+] clearance. Altogether, these data reveal a mechanism of enhanced vulnerability to ischemic injury linked to abnormal extracellular ion homeostasis and susceptibility to ischemic depolarizations in CADASIL., Introduction Cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL) is the most common monogenic small vessel disease, characterized by frequent migraine attacks with aura, progressive white matter degeneration, and [...]

Spreading depolarizations are highly prevalent and spatiotemporally punctuated events worsening the outcome of brain injury. Trigger factors are poorly understood but may be linked to sudden worsening in supply-demand mismatch in compromised tissue. Sustained or transient elevations in intracranial pressure are also prevalent in the injured brain. Here, using a mouse model of large hemispheric ischaemic stroke, we show that mild and brief intracranial pressure elevations (20 or 30 mmHg for just 3 min) potently trigger spreading depolarizations in ischaemic penumbra (4-fold increase in spreading depolarization occurrence). We also show that 30 mmHg intracranial pressure spikes as brief as 30 s are equally effective. In contrast, sustained intracranial pressure elevations to the same level for 30 min do not significantly increase the spreading depolarization rate, suggesting that an abrupt disturbance in the steady state equilibrium is required to trigger a spreading depolarization. Laser speckle flowmetry consistently showed a reduction in tissue perfusion, and two-photon pO2 microscopy revealed a drop in venous pO2 during the intracranial pressure spikes suggesting increased oxygen extraction fraction, and therefore, worsening supply-demand mismatch. These haemodynamic changes during intracranial pressure spikes were associated with highly reproducible increases in extracellular potassium levels in penumbra. Consistent with the experimental data, a higher rate of intracranial pressure spikes was associated with spreading depolarization clusters in a retrospective series of patients with aneurysmal subarachnoid haemorrhage with strong temporal correspondence. Altogether, our data show that intracranial pressure spikes, even when mild and brief, are capable of triggering spreading depolarizations. Aggressive prevention of intracranial pressure spikes may help reduce spreading depolarization occurrence and improve outcomes after brain injury. [ABSTRACT FROM AUTHOR]

Byline: Homa. Sadeghian, Rouzbeh. Motiei-Langroudi Background: Migraine is a chronic and disabling disorder. Treatment of migraine often comprises of symptomatic (abortive) and preventive (prophylactic) treatment. The current drugs used in [...]

Oedema refers to the excessive accumulation of fluid within intercellular tissues as a result of disequilibrium between the capillary hydrostatic and oncotic pressure gradients. Lumbar disc herniation (LDH) commonly causes lower back pain and radicular leg pain. We report a 57-year-old female who presented to the neurosurgery clinic of the Bam University of Medical Sciences, Bam, Iran, in 2015 with pain and pitting oedema in the bilateral lower extremities. Magnetic resonance imaging confirmed a diagnosis of LDH of the L3–L4 and L4–L5 vertebrae. The patient subsequently underwent a bilateral laminotomy and foraminotomy of the involved vertebrae to relieve her pain. Following the surgery, there was a complete resolution of the LDH-related symptoms as well as the oedema. Although LDH has never before been associated with oedema, it may nevertheless cause lower limb oedema in exceptional and rare cases, as highlighted in this patient. [ABSTRACT FROM AUTHOR]

Study Design Retrospective study. Purpose To evaluate how motor, sensory, and urinary outcomes of spinal cord injury (SCI) patients were influenced in the long term. Overview of Literature SCI is a potentially disabling and devastating neurological outcome that can occur because of spinal column fractures. Most studies have not evaluated or have failed to show the influence of different surgical approaches and other parameters on neurological recovery. Methods: A thorough history regarding sensory, motor, and urinary complaints was taken from 103 patients with SCI due to vertebral fracture; patients were followed by a thorough neurological examination. Subsequently, all medical records of patients, including neurological state after trauma, trauma mechanism, treatment protocol, surgical protocol, and imaging findings, were evaluated. Results: Of the 103 patients, 73.8% were survivors of a major earthquake and 26.2% were victims of vehicle accidents; 92.2% patients were surgically treated, while 7.8% underwent conservative management. The mean follow-up duration was 10.3 years. In follow-up visits, 67.0%, 12.6%, 13.6%, and 6.8% patients showed no, partial, substantial, and complete motor improvement, respectively; 68.0%, 26.2%, and 5.8% showed no, mild, and substantial sensory improvement, respectively; and 73.8%, 17.5%, and 8.7% showed no, substantial, and complete urinary improvement, respectively. Logistic regression analysis showed that sex, age at injury time, follow-up duration, trauma mechanism, and stem cell therapy had no effect on motor, sensory, and urinary improvement. Higher initial scores on the American Spinal Injury Association (ASIA) classification, lumbar fracture level, and performance of laminectomy improved motor outcome; higher initial ASIA scores improved urinary and sensory outcomes. Conclusions: The initial ASIA score is the most important factor for prognosticating motor, sensory, and urinary improvement in SCI patients. Lumbar (L3–L5) and thoracic (T1–T10) fractures have the best and worst prognosis, respectively, in terms of motor recovery. Laminectomy during surgery improves motor function.

The underlying structure of National Institutes of Health Stroke Scale (NIHSS) as the most widely used scale in clinical trials has been the focus of little attention. The aim of the current study was to elucidate the clustering pattern of NIHSS items in ischemic stroke patients. A series of 152 consecutive patients with first-ever ischemic strokes admitted to a university affiliated hospital were enrolled. NIHSS score was estimated on admission and correlation coefficients between its items were calculated. Further, exploratory factor analysis was used to study the clustering pattern of NIHSS items. Extinction neglect, visual field, and facial palsy were weakly associated with other NIHSS items. Factor analysis led to a four-factor structure. Factors 1 and 3 were determined by left brain function as items of right arm and leg motor, language and dysarthria loaded on both of them. By contrast, factor 2 reflected right brain involvement. Since visual field and ataxia loaded on factor 4, this factor was primarily associated with posterior strokes. Our study shows that a four-factor structure model is plausible for NIHSS. Further, for the first time, a single distinct factor is identified for posterior strokes. [ABSTRACT FROM AUTHOR]

Cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL) is the most common monogenic form of small vessel disease characterized by migraine with aura, leukoaraiosis, strokes, and dementia. CADASIL mutations cause cerebrovascular dysfunction in both animal models and humans. Here, we showed that 2 different human CADASIL mutations (Notch3 R90C or R169C) worsen ischemic stroke outcomes in transgenic mice; this was explained by the higher blood flow threshold to maintain tissue viability compared with that in wild type (WT) mice. Both mutants developed larger infarcts and worse neurological deficits compared with WT mice, regardless of age or sex after filament middle cerebral artery occlusion. However, full-field laser speckle flowmetry during distal middle cerebral artery occlusion showed comparable perfusion deficits in mutants and their respective WT controls. Circle of Willis anatomy and pial collateralization also did not differ among the genotypes. In contrast, mutants had a higher cerebral blood flow threshold, below which infarction ensued, suggesting increased sensitivity of brain tissue to ischemia. Electrophysiological recordings revealed a 1.5- to 2-fold higher frequency of peri-infarct spreading depolarizations in CADASIL mutants. Higher extracellular K+ elevations during spreading depolarizations in the mutants implicated a defect in extracellular K+ clearance. Altogether, these data reveal a mechanism of enhanced vulnerability to ischemic injury linked to abnormal extracellular ion homeostasis and susceptibility to ischemic depolarizations in CADASIL. [ABSTRACT FROM AUTHOR]

Aim: Pineal tumors represent uncommon intracranial tumors with highly diverse histologic subtypes. There still exists a controversy in literature about what influences overall survival and outcome., Material and Methods: We present the results of 48 patients with pineal tumor treated either by stereotactic biopsy followed by adjuvant therapy (23 patients) or open surgical resection without (18 patients) or with (7 patients) adjuvant therapy in Shohada Tajrish Hospital, Iran (1993-2008)., Results: Unremarkable pathology yield was 3/23 in the biopsy and 1/25 in the surgical group. Perioperative mortality and morbidity were 4.3% and 0% in the biopsy group and 32.0% and 4.0% in the surgical group. Analysis showed that age, gender, cranial nerve deficit, motor deficit, preoperative Karnofsky Performance Score (KPS), midbrain involvement, and brain stem involvement had no effect on neither perioperative mortality nor long-term survival, while local invasion and pineocytoma pathology increased perioperative mortality and presence of hydrocephalus and pineoblastoma pathology significantly decreased long-term survival. Hospitalization length was shorter in the stereotactic biopsy plus adjuvant therapy group., Conclusion: The results of the study suggests that although gross total resection is the standard of care in most pineal tumors nowadays, stereotactic biopsy followed by adjuvant therapy may still be a safe and viable option.