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Biomedical subjects

Y-W Cho

Publications and source records attributed to Y-W Cho.

5 recordsLinked to original sources
PubMed2006

Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns.

OBJECTIVE: To determine the frequency of cerebellar infarction mimicking vestibular neuritis (VN), the pattern of clinical presentation, and the territory of the cerebellar infarction when it simulates VN. METHODS: We studied 240 consecutive cases of isolated cerebellar infarction in the territories of the cerebellar arteries diagnosed by brain MRI from the acute stroke registry at the Keimyung University Dongsan Medical Center. RESULTS: We identified 25 patients (10.4%) with isolated cerebellar infarction who had clinical features suggesting VN. Two types of cerebellar infarction simulating VN were found: isolated spontaneous prolonged vertigo with imbalance as a sole manifestation of cerebellar infarction (n = 24) and isolated spontaneous prolonged vertigo with imbalance as an initial manifestation of cerebellar infarction (n = 1) followed by delayed neurologic deficits 2 days after the onset. The cerebellar infarction territory most commonly involved was the medial branch of the posterior inferior cerebellar artery territory (24/25: 96%), followed by the anterior inferior cerebellar artery territory (1/25: 4%). None of patients with infarcts in the territory of the superior cerebellar artery or multiple cerebellar arteries showed isolated spontaneous prolonged vertigo. CONCLUSIONS: Cerebellar infarction simulating vestibular neuritis is more common than previously thought. Early recognition of the pseudo-vestibular neuritis of vascular cause may allow specific management.

Adult↗
PubMed2003

Roles of protein kinase A and C in the opioid potentiation of the GABAA response in rat periaqueductal gray neuron.

The periaqueductal gray (PAG) is the main target site of the opioid-induced analgesia. The present study was designed to examine the roles of protein kinase A (PKA) and C (PKC) in the opioid-induced modulation of the currents activated by an inhibitory neurotransmitter, gamma-aminobutyric acid (GABA). The PAG neurons were acutely isolated and voltage-clamped under the nystatin-perforated patch-clamp mode. The GABA-activated current was sensitively blocked by a GABA(A) receptor antagonist, bicuculline, and selectively carried by chloride ions. The GABA(A) receptor-activated Cl(-) current was potentiated by a mu-opioid receptor agonist, [D-Ala(2),N-MePhe(4),Gly(5)-ol]-enkephalin acetate (DAMGO). The GABA response was also potentiated by phorbol-12-myristate-13-acetate (PMA). Pretreatment with PMA occluded the DAMGO potentiation. However, both chelerythrine and 2-[1-(3-dimethylaminopropyl)indol-3-yl]-3-(indol-3-yl) maleimide (GF109203X) also potentiated the GABA response. Pretreatment with chelerythrine or GF109203X also occluded the DAMGO potentiation. Meanwhile, the GABA response was potentiated by N-(2-[p-bromocinnamylamino]-ethyl)-5-isoquinolinesulfonamide (H-89), while not altered by forskolin. Pretreatment with H-89 occluded the potentiation effect of DAMGO on the GABA response. In addition, the DAMGO effect was completely blocked by pretreatment with forskolin. From the result, it can be suggested that activation of mu-opioid receptor potentiates the GABA(A) response through the mediation of PKA inhibition, and that PKC is not directly involved in the action mechanism of DAMGO.

Animals↗
PubMed2003

Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction.

OBJECTIVES: To investigate the clinical and radiological features of patients presenting with an acute auditory syndrome as a prodromal symptom of anterior inferior cerebellar artery (AICA) infarction. METHODS: 16 consecutive cases of AICA infarction diagnosed by brain magnetic resonance imaging completed a standardised audiovestibular questionnaire and underwent a neuro-otological evaluation by an experienced neuro-otologist. RESULTS: Five patients (31%) had an acute auditory syndrome as a prodrome of AICA infarction one to 10 days before onset of other brain stem or cerebellar symptoms. Two types of acute auditory syndrome were found: recurrent transient hearing loss with or without tinnitus (n = 3), and a single episode of prolonged hearing loss with or without tinnitus (n = 2). The episodic symptoms were brief, lasting only minutes. The tinnitus preceding the infarction was identical to the tinnitus experienced at the time of infarction. At the time of infarction, all patients developed hearing loss, tinnitus, vertigo, and ipsilateral hemiataxia. The most commonly affected site was the middle cerebellar peduncle (n = 5). Four of the five patients had incomplete hearing loss and all had absence of vestibular function to caloric stimulation on the affected side. CONCLUSIONS: Acute auditory syndrome may be a warning sign of impending pontocerebellar infarction in the distribution of the AICA. The acute auditory syndrome preceding an AICA infarct may result from ischaemia of the inner ear or the vestibulocochlear nerve.

Acute Disease↗