Background: Ketamine is rarely used alone because of its association with poor muscle relaxation, tachycardia, catalepsy or muscle rigidity and therefore commonly used in combination with alpha 2 agonist or opioid to minimize the untoward effects. The aim of the present anaesthetic study was to evaluate the clinico-physiological effects of ketamine alone and in combination with dexmedetomidine or butorphanol for inducing adequate anaesthesia in dogs. Methods: The present anaesthetic study was conducted on 18 (eighteen) healthy dogs of either sex and randomly divided into three groups (K, DK and BK) with six animals in each group. Atropine sulphate @ 0.04 mg/ kg was administered intramuscularly 15 minutes prior to anaesthetic study to all the animals. In group K, ketamine HCl alone was administered @ 5 mg/kg by slow i/v and kept as control. In group DK and BK, after administration of atropine sulphate 15 minutes later dexmedetomidine @ 10 µg/kg i/m and butorphanol @ 0.2 mg/kg i/m were administered respectively. Ten minutes later ketamine HCl was administered @ 5 mg/kg slowly intravenously in both group DK and BK to induce surgical stage of general anaesthesia. The following clinical parameters were recorded viz., onset of sedation, onset of anaesthesia, degree of analgesia, extent of muscle relaxation, duration of anaesthesia and complete recovery. The physiological parameters (rectal temperature, heart rate and respiratory rate) were recorded before anaesthetic study at 0 min. and at 10 minutes after preanaesthetic administration and then at 10, 20, 40, 60, 90, 120 and 180 minutes after ketamine anaesthesia. All the data were analyzed using SPSS v 15.0 statistics software program and presented as mean±Standard Error. Result: The onset of sedation was quicker in group DK followed by group K and BK. Duration of anaesthesia and complete recovery in group DK was significantly (p less than 0.01) longer than in group K and BK. The degree of analgesia was excellent in group DK and good in group K and BK. The extent of muscle relaxation was excellent in group DK, good in group BK and was poor in group K. The physiological parameters showed transient changes which compensated and remained within normal range during the observation period. The above anaesthetic study suggests that ketamine in combination with dexmedetomidine or butorphanol can be safely used for inducing adequate anaesthesia in dogs. However, dexmedetomidine-ketamine can be used safely for longer duration of surgical procedures in dogs.

Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy are characterized by aggregation of abnormal α-synuclein (α-syn) and collectively referred to as α-synucleinopathy. Because these diseases have different prognoses and treatments, it is desirable to diagnose them early and accurately. However, it is difficult to accurately diagnose these diseases by clinical symptoms because symptoms such as muscle rigidity, postural dysreflexia, and dementia sometimes overlap among these diseases. The process of conformational conversion and aggregation of α-syn has been thought similar to that of abnormal prion proteins that cause prion diseases. In recent years, in vitro conversion methods, such as real-time quaking-induced conversion (RT-QuIC), have been developed. This method has succeeded in amplifying and detecting trace amounts of abnormal prion proteins in tissues and central spinal fluid of patients by inducing conversion of recombinant prion proteins via shaking. Additionally, it has been used for antemortem diagnosis of prion diseases. Recently, aggregated α-syn has also been amplified and detected in patients by applying this method and many clinical studies have examined diagnosis using tissues or cerebral spinal fluid from patients. In this review, we discuss the utility and problems of α-syn RT-QuIC for antemortem diagnosis of α-synucleinopathies.

Abstract Background: Parkinson's disease (PD) is associated with the destruction of dopaminergic neurons in the substantia nigra (SN). Hydroxychloroquine (HCQ) has the capability to cross the blood-brain barrier and promote a neuroprotective potential. This study evaluated the effects of HCQ on the 6-hydroxydopamine (6-OHDA)-induced PD model in rats.Methods: Wistar rats were randomly divided into sham, PD, PD+levodopa, and PD+HCQ groups. The PD model was induced by a stereotactic administration of 6-OHDA into the left SN pars compacta (SNpc) and confirmed by rotation and the Murprogo’s tests. HCQ (100 mg/kg, p.o.) and levodopa (12 mg/kg, p.o.) were administered once a day for 21 days. Three weeks after surgery, the behavioral tests were performed. Brain lipid peroxidation index (MDA), glutathione peroxidase activity (GPx), total antioxidant capacity (TAC) levels, and α-synuclein protein expression in the SN were also measured. Results: The behavioral tests demonstrated that induction of PD increased the muscle rigidity and the number of rotations, which were reversed by HCQ treatment. Also, induction of PD was associated with an increase in α-synuclein protein levels and MDA and decreased TAC levels and GPx activity. However, HCQ decreased α-synuclein and MDA levels while increased TAC levels and GPx activity. Additionally, histopathological data showed that HCQ protects dopaminergic neurons against 6-OHDA-induced toxicity.Conclusion: According to the results, HCQ has a beneficial effect in improving PD-related pathophysiology, in part, by mitigating oxidative stress and protecting the dopaminergic neurons in the SN.

Malignant hyperthermia (MH) is a potentially fatal hypermetabolic syndrome that occurs when susceptible individuals are exposed to triggering agents. Variability in the order and time of occurrence of symptoms often makes clinical diagnosis difficult. A late diagnosis or misdiagnosis of delayed-onset MH may lead to fatal complications. We herein report a case of delayed-onset MH in the postoperative recovery room. A 77-year-old man awoke from anesthesia and was transferred to the recovery room. Ten minutes after his arrival, his mental status became stuporous and he developed masseter muscle rigidity, hyperventilation, and a body temperature of 39.8°C. The patient was suspected to have MH, and 60 mg of dantrolene sodium (1 mg/kg) was administered via intravenous drip with symptomatic treatment. Within 10 minutes of dantrolene administration, the patient’s clinical signs subsided. This case report demonstrates that rapid diagnosis and treatment are crucial to ensure a good prognosis for patients with MH. A high level of suspicion based on clinical symptoms and early administration of therapeutic drugs such as dantrolene will also improve the clinical course. Therefore, suspicion and prompt diagnosis are absolutely essential. This case report emphasizes the importance of continuous education in the diagnosis and treatment of MH.

Abstract We present a case in which a patient developed fever and leukocytosis subsequent to each monthly haloperidol decanoate injection, an adverse reaction that does not meet the diagnostic criteria of neuroleptic malignant syndrome (NMS) or any previously reported adverse reaction for this medication. A patient being treated with haloperidol decanoate for psychosis experienced a fever within 3 days of injection and leukocytosis along with swelling, pain, and a “knot” feeling at the injection site. This recurred after each injection for several months. Muscle rigidity or changes in vital signs other than temperature were not noted. Temperature and injection site reactions resolved with administration of acetaminophen and ibuprofen. The elevation in temperature was discovered as a result of universal twice daily temperature monitoring implemented due to the COVID-19 pandemic. Reports of fever with antipsychotics are typically associated with NMS or heat stroke; the details of this case do not meet the clinical criteria for either. Similar reactions are reported for other antipsychotics, such as clozapine and olanzapine, but not for haloperidol. The recommendation was to discontinue use of the medication due to an unclear mechanism of the reaction.

Neuroleptic Malignant Syndrome (NMS) is a medical emergency of infrequent presentation in Emergency department, which is associated with the use of psychotropic agents, classical and atypical antipsychotics. We report a case involving a 56-year-old male patient diagnosed with schizophrenia and depression for 30 years, who had been receiving Amisulpride, Trifluoperazine, Clozapine, and Amitryptiline as part of his treatment. This patient presented with symptoms of NMS with fever, muscle rigidity, altered mental state, elevated CPK, Urea, and S. Creatinine levels. NMS may be responsible for serious rhabdomyolysis, acute respiratory distress syndrome, and disseminated intravascular coagulation. We hypothesize the occurrence of acute renal failure precipitated by NMS. His treatment included the withdrawal of all psychotropic agents, Bromocriptine, and other supportive measures.

Under this name Schanz (Die Lehre von den statischen Insufficienterkrankungen usw, Stuttgart, 1921) tries to substantiate a new nosological form, by which he understands a primary disease of the spine, arising on the basis of static overburdening and manifested clinically by a feeling of fatigue, pain, and also inflammatory phenomena: edema , muscle rigidity, etc. phenomena.

Pain management is necessary for all surgical procedures. Little scientific evidence about drug efficacy in donkeys is available. The aim of this study was to evaluate the analgesic effect of butorphanol in donkeys undergoing orchiectomy under total intravenous anaesthesia with guaifenesin-ketamine-detomidine. A randomized blinded prospective clinical trial (Protocol n. 2021/0000338), was carried out on 18 clinically healthy donkeys undergoing bilateral orchiectomy. Patients were assigned to Group D (n = 8) or Group DB (n = 10) if receiving intravenous detomidine or detomidine-butorphanol respectively, before induction of general anaesthesia with ketamine-diazepam. Intraoperative muscle relaxation, nystagmus, palpebral reflex, heart and respiratory rate, and non-invasive blood pressure were evaluated every 2 min; time to prepare the patient, duration of surgery and anaesthesia and recovery score were recorded. Group D had significantly longer surgical time, higher heart rate, higher systolic and mean blood pressure (p < 0.05; repeated measure ANOVA), increased muscle rigidity and expression of palpebral reflex (p < 0.05; Mann–Whitney U test) than group DB. Top-ups with thiopental were statistically higher in Group D. Butorphanol and detomidine together produced a more stable anaesthetic plan. The low dosage of opioid and alpha-2-agonists and reduced rescue anaesthesia are responsible for a safer and more superficial anaesthesia, which is mandatory under field conditions.

Parkinson’s disease (PD), a neurodegenerative disease is becoming major health concern mainly for elder people of age over 60 years. The main cause of PD is permanent loss/death of dopaminergic nerve cells present in brain part called substantia nigra, which is responsible for dopamine synthesis. MAO-B, monoamine oxidase B, regulates dopamine metabolism and increased activity of MAO-B causes dopamine degradation which in turn promotes the accumulation of glutamate and oxidative stress with free radical liberation. Several factors like oxidative stress, free radical formation, increased cholesterol, mitochondrial dysfunction, nitric oxide toxicity, signal-mediated apoptosis, head trauma, and environmental toxins and gene mutations like VPS35, SNCA, EIF4G1, GBA, CHCHD, LRRK2, PINK1, DNAJC13 and SOD2 are associated with PD. Symptoms of PD include bradykinesia, muscle rigidity, resting tremors, postural instability and shuffling gait, constipation, sleep problems, fatigue, apathy, loss of smell and taste, excessive sweating, frequent nightmares, dream enacting behaviour, anxiety, depression, daytime drowsiness. In PD, low levels of ceruloplasmin were observed in people with early onset of PD. Ceruloplasmin, a ferroxidase enzyme which is synthesized in liver parenchymal cell, regulates iron metabolism and lower level of which causes iron accumulation in brain which is responsible for the early onset of PD. Levodopa-based preparations, Dopamine agonists, Catechol-o-methyltransferase (COMT) inhibitors, MOA-B inhibitors, Adjunctive therapy, Antiglutamatergics drugs are currently used for the treatment of PD.