Safety and clinical outcomes of urgent superficial temporal artery-middle cerebral artery bypass-a single-institution retrospective analysis.

BACKGROUND: Intravenous recombinant tissue-type plasminogen activator (rt-PA) with/without endovascular treatment is sometimes not ideally effective for the treatment of acute hemodynamic stroke due to atherosclerotic major artery steno-occlusive disease, and some patients show fluctuation in or progression of symptoms despite intensive medical therapy. Urgent superficial temporal artery-middle cerebral artery (STA-MCA) bypass has been reported to be effective in patients with progressing stroke. OBJECTIVE: To investigate the efficacy of urgent STA-MCA bypass performed at a single institution for progressing stroke due to hemodynamic compromise caused by atherosclerosis. METHOD: We retrospectively reviewed clinical and operative records. Neurological outcomes were assessed with the modified Rankin Scale (mRS) with consideration of patient age: more than 2 points on the mRS was regarded as a poor outcome in patients under 80 years old, and more than 3 points was considered a poor outcome in those over 80 years old. The risk factors contributing to poor outcomes were evaluated. RESULTS: From 2008 to 2017, 35 patients underwent urgent STA-MCA bypass for progressing stroke. The average patient age was 70.4 years (range 49-96 years). The mean National Institutes of Health Stroke Scale (NIHSS) score was 5.1 (range 0-24 points) on admission and 7.8 before surgery. After 3 months, 25 patients showed good outcomes. The preoperative NIHSS score contributed to a poor outcome (odds ratio 1.65 (95% confidence interval 1.12-2.90)). CONCLUSIONS: Urgent STA-MCA bypass is a treatment option for patients with progressing stroke. The operation should be performed while the NIHSS score is low.

Safety of urgent STA-MCA anastomosis after intravenous rt-PA treatment: a report of five cases and literature review.

BACKGROUND: Intravenous recombinant tissue-type plasminogen activator (rt-PA) with/without endovascular treatment is not as effective in atherosclerotic steno-occlusive acute ischemic stroke. Urgent superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis is effective to some extent in progressing stroke, but the safety of STA-MCA anastomosis soon after rt-PA therapy is unknown. Our aim was to clarify the safety of STA-MCA anastomosis within 24 h after intravenous rt-PA. METHOD: From 2005 to 2015, rt-PA was administered to 225 patients presenting with acute ischemic stroke according to the Japanese Stroke Guidelines, in our institution. Five patients underwent urgent STA-MCA anastomosis after rt-PA administration with or without endovascular recanalization. Clinical time course, surgical complications, and patients' prognosis were investigated. RESULTS: The average of patient age was 65.4 years (range 49-77 years); three patients had internal carotid artery occlusion, and two patients had middle cerebral artery occlusion. The median National Institutes of Health Stroke Scale score on admission was 12.4 (range 6-17 points) and operation occurred 10.6 h (range 5.3-23.6 h) after intravenous rt-PA administration. Hemostasis was achieved during standard STA-MCA anastomosis, and there were no hemorrhagic complications. CONCLUSIONS: In our consecutive cases, urgent STA-MCA anastomosis after at least 5.3 h after intravenous rt-PA was performed safely without hemorrhagic complications.

Ipsilateral sensorimotor deficits in lateral medullary infarction: a case report.

The patient, a 32-year-old man, presented with sudden onset of occipital headache, vertigo, dysarthria, gait ataxia, right Horner syndrome, numbness of the right hand, and mild right hemiparesis. On magnetic resonance imaging, an acute small infarction was located on the right side of the caudal medulla extending dorsomedially. Magnetic resonance angiography showed severe right vertebral artery stenosis. Lateral medullary infarction associated with ipsilateral sensorimotor deficits in the limb is very rare, and the lesion probably involved the ipsilateral dorsal column or decussating lemniscal fibers and corticospinal fibers caudal to the pyramidal decussation or compression of the decussation.

[A 64-year-old male with recurrence of herpes simplex encephalitis after suffering from severe pneumonia and sepsis].

The case is a 64-year-old male who had a past history of herpes simplex virus encephalitis (HSE) two years prior to his admission. He was admitted to our hospital due to severe pneumonia and sepsis. Several days later, he developed HSE again. It has been known that immunosuppressive state called immune paralysis occurs in the patient with sepsis due to the amplification of anti-inflammatory responses after the initial hyper-inflammatory phase, which increases the susceptibility to various latent viruses including herpes simplex virus. In the present case, we consider that the severe infection may trigger the recurrence of HSE through the viral reactivation due to immune paralysis. When we see a patient suffering from severe infection who had a past history of HSE, we should keep in mind that such a patient may have a risk of the recurrence of HSE.

Reduction in the motor unit number estimate (MUNE) after cerebral infarction.

BACKGROUND: The mechanism of the decrease in motor unit number estimates (MUNEs) after cerebral infarction has not been studied systematically. We examined the relationship between the degree to which MUNEs decreased and the other clinical features of patients with the infarction. METHODS: Using a multiple point stimulation technique, we obtained the MUNE of the hypothenar muscle group in 13 age-matched control subjects and 30 patients with cerebral infarction. In all patients, we obtained the Japan Stroke Scale (JSS) and head MR images. In eight patients with acute cerebral infarction, admitted within 24 h after onset, we also obtained head MR angiograms and single-photon emission CT. FINDINGS: There was a decrease in the MUNE of the hypothenar muscle group on the affected side of 24 patients with cerebral infarction and hand weakness. The decrease in the MUNE started from 4 to 30 h after the infarction, when T1-weighted MR images of the brain involved were normal. The degree to which the MUNE decreased correlated with the part of the JSS showing the upper extremity weakness. INTERPRETATIONS: A decrease in the MUNE of the hypothenar muscle group within 30 h after cerebral infarction may be due to trans-synaptic inhibition of the spinal alpha motor neurons innervating this muscle.

Cheiro-oral-pedal syndrome due to brainstem hemorrhage.

Cheiro-oral-pedal syndrome is characterized by specific sensory disturbance around the corner of the mouth, in the hand and in the foot on the same side. Lesions responsible for causing this syndrome vary. We report two cases of cheiro-oral-pedal syndrome due to midbrain and pontine hemorrhage, respectively. Pontine hemorrhage producing cheiro-oral-pedal syndrome has been reported in three cases, but this is the first case that midbrain hematoma exhibits this syndrome. Damage in the sensory pathway can cause cheiro-oral-pedal syndrome. Difference in the threshold may explain the specific sensory pattern in this syndrome. Cheiro-oral-pedal syndrome is caused by lacunar infarction in majority of the cases. However, it should be kept in mind that hematomas can cause cheiro-oral-pedal syndrome.

Cheiro-pedal syndrome following pontine infarction.

We report the case of a 64-year-old man with sudden onset of numbness in the right hand and foot. Neurological examinations were normal except for hypersthesia, and hyperalgesia of the right hand and foot. Brain MRI demonstrated a high signal intensity on T2-weighted image and a low signal intensity on T1-weighted image in the left tegmetum of the pons. He was diagnosed with pontine infarction presenting with cheiro-pedal syndrome (CPS). Damage in the sensory pathways can cause CPS. Difference in the threshold may explain the specific sensory pattern in this syndrome. Further examination of the relationship between sensory symptoms and localization on MRI is needed to clarify this syndrome.

Steroids and Immunosuppressant Agents Do Not Affect Indirect Revascularization in Quasi-Moyamoya Disease Associated with Pure Red Cell Aplasia: A Case Report.

A 31-year-old woman with pure red cell aplasia presented with motor aphasia and right homonymous hemianopia due to a left temporal and parietal lobe infarction. Magnetic resonance angiography revealed an occlusion of the left anterior and middle cerebral artery, with the development of moyamoya vessels. She was diagnosed with quasi-moyamoya disease and subsequently underwent direct and indirect anastomosis surgery, while continuing steroid and immunosuppressant therapy for pure red cell aplasia. The postoperative course was uneventful, and follow-up cerebral angiography 6 months after the surgery revealed the development of neovascularization through an indirect anastomosis. Neovascularization can be induced while the patient is receiving steroid and immunosuppressant therapy in quasi-moyamoya disease.

Ulcerative colitis presenting as sensorineural deafness, brainstem encephalopathy, and white matter lesions.

BACKGROUND: Several rare neurologic complications of ulcerative colitis have been reported. REVIEW SUMMARY: We report a 69-year-old Japanese woman who developed bilateral sensorineural deafness, 2 attacks of bilateral ophthalmoplegia, and bilateral facial nerve palsy in association with ulcerative colitis. Laboratory data showed elevated cerebrospinal fluid (CSF) protein without pleocytosis, abnormal auditory brainstem evoked potentials, and multiple high signal lesions on magnetic resonance imaging of the brainstem and cerebral deep white matter. Her symptoms improved with corticosteroid therapy except for sensorineural deafness and an exacerbation of cerebral deep white matter lesions without any new clinical signs. CONCLUSION: Immunologic mechanisms may have led to her central and peripheral nervous system findings in addition to her colon disorder.

Trophic effect of olmesartan, a novel AT1R antagonist, on spinal motor neurons in vitro and in vivo.

Olmesartan is a novel compound which has been shown to exhibit various neuropharmacological effects. For the purpose of clarifying the effect of Olmesartan on spinal motor neurons, we studied the following tests. We studied the effect in vitro of Olmesartan on neurite outgrowth and choline acetyltransferase (ChAT) activity in primary explant cultures of ventral spinal cord (VSCC) of fetal rats. Olmesartan-treated VSCC, compared with control VSCC, had a significant neurite outgrowth and increased activity of ChAT. The effect was dose-related in neurite outgrowth. However, there was no relationship between activity of ChAT andgiven doses of Olmesartan. We examined in vivo the effect of Olmesartan on axotomized spinal motor neuron death in the rat spinal cord. After post-natal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of Olmesartan for consecutive 14 days reduced spinal motor neuron death. There was no relationship between number of surviving neurons and doses of Olmesartan. These in vitro and in vivo studies showed that Olmesartan has a neurotrophic effect on spinal motor neurons. Our data suggest a potential therapeutic use of Olmesartan in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Protective effect of interleukin-3 and erythropoietin on motor neuron death after neonatal axotomy.

Several members of hematopoietic factors are known to have neuroprotective effects against axotomized motor neuron death. We carried out a study to determine whether interleukin-3 (IL-3) and erythropoietin (EPO) rescue spinal motor neuron death following axotomy. Unilateral sciatic nerve was transected in neonatal rats. Different doses of IL-3, EPO, or vehicle were administered daily for two weeks by intraperitoneal injection. After treatment, the number of spinal motor neurons was determined at the level of L4 segment In comparison with vehicle, both IL-3 (10 microg kg(-1)) and EPO (5.0 mg kg(-1)) significantly prevented the loss of motor neurons. Protective potentials is the same between them. These results suggest that IL-3 and EPO play a role for motor neuron survival in vivo and suggest the potential use of these hematopoietic factors in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Neuroprotective actions of FK506 and cyclosporin A on motor neuron survival following neonatal axotomy.

We show that nonimmunosuppressive analogues of the immunosuppressive drugs FK506 and cyclosporin A (CsA) rescue axotomized neonatal motor neuron death. Unilateral sciatic nerve was transected in neonatal rats. Animals were then treated daily with different doses of FK506 and CsA for 14 days with intraperitoneal injection. Control rats received phosphate buffer saline (PBS) in the same fashion. After treatment, the number of spinal motor neurons was determined at L4 level. In comparison with vehicle, both FK506 (5.0 mg kg(-1)) and CsA (10.0 mg kg(-1)) rescued motor neuron death in a similar way. These results indicate therapeutic relevance in the treatment of damaged motor neuron disorders, such as motor neuropathy or amyotrophic lateral sclerosis.

Temocapril prevents motor neuron damage and upregulation of cyclooxygenase-II in glutamate-induced neurotoxicity.

To examine the possible neuroprotective effect of temocapril, one kind of angiotensin-converting enzyme inhibitor, against glutamate-induced neurotoxicity, we analyzed the pharmacologic utility of temocapril in a post-natal organotypic culture model of motor neuron degeneration. Treatment with 10(-5) M of glutamate resulted in a motor neuron loss and decreased activity of choline acetyltransferase (ChAT). Cotreatment of 10(-5) M of glutamate and temocapril revealed protective effect on motor neuron death and decreased activity of ChAT. Next we performed reverse transcription-PCR analysis for cyclooxygenase-II (COX-II). COD-II mRNA was upregulated in glutamate-treated culture. Cotreatment with temocapril and glutamate inhibited upregulation of COX-II. Taken together, temocapril may have therapeutic potential for diseases which associate with upregulation of COX-II, in addition to its role in glutamate excitotoxicity.

The diagnostic interval in amyotrophic lateral sclerosis.

We studied whether there are any parameters that influence the period between onset of symptoms and confirmation of diagnosis in 117 patients with ALS (65 male, 52 female). The mean age of diagnosis was 57 years for men and 59 years for women. Bulbar-onset patients were older at diagnosis than limb-onset patients both men and women. Patients with bulbar-onset appeared to be more frequent in women (33:19). Contrariwise, limb-onset patients were more frequently male (43:22). The time to confirmation was much shorter with symptoms of bulbar-onset (10.5 months in male, 9.8 months in female) than for those with limb-onset (13.7 months in male, 14.8 months in female) in male, respectively, female ALS patients. The diagnosis of ALS was established in all cases by neurologists in our study.

Unusual fatty infiltration of the soleus muscle in a patient with congenital nemaline myopathy: fat-suppression muscle MRI.

A 27-year-old man developed gait disturbance over a three-year period. Histochemical analysis suggested nemaline bodies, type I fiber atrophy and type II fiber hypertrophy. Conventional magnetic resonance imaging (MRI) showed a severe degree of homogenous hyperintensity in the soleus muscle. Fat-suppression MRI exhibited marked diffuse hypointensity in the soleus muscle. MRIs demonstrated unusual fatty proliferation of the soleus muscle. Fat-suppression MRI of skeletal muscles is beneficial in evaluating the accurate topography and degree of fatty infiltration. Radiological patterns of muscle damage are variable in patients with congenital nemaline myopathy, similar to the heterogeneous clinical aspects.

Acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.

Emerging sylvian subpial hematoma after the repair of the ruptured anterior cerebral artery aneurysm with interhemispheric approach: case report.

A 60-year-old woman was admitted to the hospital due to a sudden loss of consciousness. Computed tomography (CT) revealed a thick subarachnoid hemorrhage in almost all of the parachiasmatic cisterns, including the sylvian cisterns, with mild hydrocephalus. Three dimensional (3D)-CT angiography showed an irregularly shaped aneurysm at the bifurcation of the left A2 and the frontopolar artery. The aneurysm was successfully obliterated by clipping through the interhemispheric approach. CT performed immediately after the operation showed a newly formed left temporal subpial hematoma. The patient's neurological status improved gradually after surgery, but deteriorated again 2 days after the operation. CT revealed an enlarging right sylviansubpial hematoma. The subpial hematoma was rapidly removed surgically. Slight hemiparesis and impaired higher cognitive function remained after a shunt procedure for subsequent hydrocephalus. Emerging sylvian hematoma associated with a distant site of a ruptured aneurysm is extremely rare. However, adequate attention is required in cases with a thick subarachnoid hemorrhage in distant fissures.

Impact of immediate aortic repair on early and midterm neurologic status in patients with acute type a aortic dissection complicated by cerebral malperfusion.

Surgical treatment for acute type A aortic dissection (AAD) complicated by cerebral malperfusion (CM) remains debatable. Worsening of neurologic symptoms and poor quality of life after immediate surgery continue to be cause for concern. We performed immediate aortic repair followed by early rehabilitation in 10 patients with AAD complicated by CM. The early and midterm neurologic statuses were satisfactory. The immediate aortic repair did not have a negative impact on early and midterm neurologic condition in patients with AAD complicated by CM.