Mechanical thrombectomy (MT) has been demonstrated as an effective treatment for acute ischemic stroke (AIS), thanks to large vessel occlusion (LVO), especially in case of anterior cerebral artery with many randomized clinical trials (RCTs) every year. On the other hand, there is a limited number of basilar artery occlusion (BAO)-related studies which have been conducted. The fact prompts our range of case studies, which furnish BAO understanding with our experience, results and some prognosis factors of MT. This retrospective and single-center study was conducted on 22 patients who were diagnosed with BAO and underwent the treatment of MT from October 2012 to January 2018. Clinical feature such as radiological imaging, procedure complications, and intracranial hemorrhage were all documented and evaluated. All the studies' results based on performance using modified Rankin scale score (mRS) and mortality at 90 days. The results from these BAO patients study indicated that the posterior circulation Acute Stroke Prognosis Early CT Score (pcASPECTS) recorded before the intervention was 7.7 ± 1.6, while the admission National Institutes of Health Stroke Scale (NIHSS) was 17.5 ± 5.4. 15/22 cases achieved successful recanalization (TICI, Thrombolysis in Cerebral Infarction scale, of 2b-3), accounting for 68.2%. The results highlighted 50% of the favorable outcome (mRS 0-2) occupying 11 out of 22 patients in total and the overall mortality was 36.4%. The intracranial hemorrhagic complication was detected in three cases (13.6%). Placing in juxtaposition the poor-outcome group and the favorable-outcome group, we could witness statistically significant difference (P
Secondary paroxysmal dyskinesias (PxD) have been previously reported in patients with multiple sclerosis, lacunar infarcts, head trauma, metabolic disorders such as hyperglycaemia, hypocalcaemia, migraine and central nervous system (CNS) infections. The causative lesions typically involve the basal ganglia structures, medulla and rarely the spinal cord. We report two patients who presented with paroxysmal dyskinesias as the only manifestation of subcortical white-matter ischaemia. Patient 1 presented with 3-year history of paroxysmal kinesigenic dyskinesia (PKD) and patient 2 with 6-month history of paroxysmal nonkinesigenic dyskinesia (PNKD). All investigations, including CSF oligoclonal bands were negative, except for a brain MRI which showed multiple, non-enhancing subcortical white matter lacunar infarcts. Therefore, subcortical white matter ischaemia should also be included in the differential diagnosis of PxD.
The original concept of the ischaemic penumbra suggested imaging of regional cerebral blood flow and metabolism would be required to identify tissue that may benefit from intervention. Amide proton transfer magnetic resonance imaging, a chemical exchange saturation transfer technique, has been used to derive cerebral intracellular pH in preclinical stroke models and has been proposed as a metabolic marker of ischaemic penumbra. In this proof of principle clinical study, we explored the potential of this pH-weighted magnetic resonance imaging technique at tissue-level. Detailed voxel-wise analysis was performed on data from a prospective cohort of 12 patients with acute ischaemic stroke. Voxels within ischaemic core had a more severe intracellular acidosis than hypoperfused tissue recruited to the final infarct (P < 0.0001), which in turn was more acidotic than hypoperfused tissue that survived (P < 0.0001). In addition, when confined to the grey matter perfusion deficit, intracellular pH (P < 0.0001), but not cerebral blood flow (P = 0.31), differed between tissue that infarcted and tissue that survived. Within the presenting apparent diffusion coefficient lesion, intracellular pH differed between tissue with early apparent diffusion lesion pseudonormalization and tissue with true radiographic recovery. These findings support the need for further investigation of pH-weighted imaging in patients with acute ischaemic stroke.
Glutamate receptors are the integral cellular components associated with excitotoxicity mechanism induced by the ischemic cascade events. Therefore the glutamate receptors have become the major molecular targets of neuroprotective agents in stroke researches. Recent studies have demonstrated that a Group I metabotropic glutamate receptor agonist, (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG) preconditioning elicits neuroprotection in the hippocampal slice cultures exposed to toxic level of N-methyl-d-aspartate (NMDA). We further investigated the preconditioning effects of (S)-3,5-DHPG on acute ischemic stroke rats. One 10 or 100μM of (S)-3,5-DHPG was administered intrathecally to Sprague-Dawley adult male rats, 2h prior to induction of acute ischemic stroke by middle cerebral artery occlusion (MCAO). After 24h, neurological deficits were evaluated by modified stroke severity scores and grid-walking test. All rats were sacrificed and infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride staining. The serum level of neuron-specific enolase (NSE) of each rat was analyzed by enzyme-linked immunosorbent assay (ELISA). One and 10μM of (S)-3,5-DHPG preconditioning in the stroke rats showed significant improvements in motor impairment (P<0.01), reduction in the infarct volume (P<0.01) and reduction in the NSE serum level (P<0.01) compared to the control stroke rats. We conclude that 1 and 10μM (S)-3,5-DHPG preconditioning induced protective effects against acute ischemic insult in vivo.
Migraine with aura is one of the major subtypes of migraine, and can be associated with ischaemic brain infarction. Use of oral contraceptive pills (OCPs) increases the risk of infarction in this type of migraine. Seizures and migraine also have a complex relationship, one element of which is migraine- triggered seizures. We report a case of bilateral occipital lobe infarction and migraine-triggered seizures, most likely precipitated by oral contraceptive pills (OCPs) in a patient with migraine with visual aura. OCPs, triptans and ergotamines should be used cautiously in these patients. Methods of birth control other than OCPs should be considered.
Psychiatric symptoms may be related to a silent cerebral infarct, a phenomenon that has been described previously in literature. Acute psychosis or other neuropsychiatric symptoms including depression may present in stroke patients and patients with lesions either within the prefrontal or occipital cortices, or in subcortical areas such as the basal ganglia, thalamus, mid-brain, and brainstem. Psychosis in clinical stroke or in silent cerebral infarction is uncommon and not well documented in the literature. Neurological deficits are the most common presentation in stroke, and nearly a third of patients that suffer a stroke may experience psychological disorders such as depression and anxiety, related to physical disability. The present case report describes an elderly female patient who presented with hallucinations and depressive symptoms, and was discovered to have a recent right frontal brain infarction, without other significant neurological deficits.
Motor impairment is the most common and widely recognised clinical outcome after stroke. Current clinical practice in stroke rehabilitation focuses mainly on physical therapy, with no pharmacological intervention approved to facilitate functional recovery. Several studies have documented positive effects of growth hormone (GH) on cognitive function after stroke, but surprisingly, the effects on motor function remain unclear. In this study, photothrombotic occlusion targeting the motor and sensory cortex was induced in adult male mice. Two days post-stroke, mice were administered with recombinant human GH or saline, continuing for 28 days, followed by evaluation of motor function. Three days after initiation of the treatment, bromodeoxyuridine was administered for subsequent assessment of cell proliferation. Known neurorestorative processes within the peri-infarct area were evaluated by histological and biochemical analyses at 30 days post-stroke. This study demonstrated that GH treatment improves motor function after stroke by 50%-60%, as assessed using the cylinder and grid walk tests. Furthermore, the observed functional improvements occurred in parallel with a reduction in brain tissue loss, as well as increased cell proliferation, neurogenesis, increased synaptic plasticity and angiogenesis within the peri-infarct area. These findings provide new evidence about the potential therapeutic effects of GH in stroke recovery.