Diagnosis is difficult and typically done by ruling out Parkinsons Disease (PD) or Spinocerebellar ataxia (SCA). Symptoms include autonomic dysfunctions (supine hypertension and orthostatic hypotension, urinary incontinence). The disease leads to selective neuronal loss, myelin pallor, possible microglial activation and usually involves caudate, putamen, substantia nigra and cerebellum. Neuroimaging does show marked features in the putamen and 'hot cross bun' sign in the pons but these are not specific only to MSA. There are two broad groups MSA-P with more PD like features of bradykinesia and resting tremor and MSA-C with more limb/gait ataxia features. Treatment is symptomatic and definitive diagnosis is possible only post mortem (seen by high density oligodendroglial cytoplasmic inclusions).
In her seminar, Rukmani MR discussed the challenges surrounding Multiple System Atrophy (MSA). This is a relatively rare disorder (1.9 to 4.9 per 100,000), has an adult onset. NIMHANS gets a few cases every month.
Diagnosis is difficult and typically done by ruling out Parkinsons Disease (PD) or Spinocerebellar ataxia (SCA). Symptoms include autonomic dysfunctions (supine hypertension and orthostatic hypotension, urinary incontinence). The disease leads to selective neuronal loss, myelin pallor, possible microglial activation and usually involves caudate, putamen, substantia nigra and cerebellum. Neuroimaging does show marked features in the putamen and 'hot cross bun' sign in the pons but these are not specific only to MSA. There are two broad groups MSA-P with more PD like features of bradykinesia and resting tremor and MSA-C with more limb/gait ataxia features. Treatment is symptomatic and definitive diagnosis is possible only post mortem (seen by high density oligodendroglial cytoplasmic inclusions). Dr Jyothi (PhD Scholar) presented her seminar on "Intersection of Buddhist Meditation and Neurosciences".
She presented an overview of meditation and a variety of meditative practices and highlighted that the term meditation is very loosely used to cover very different practices (ranging from focus on breathing to exercises to dhikr chanting of Sufis) that have correspondingly different effects on the body and mind. Jyothi then introduced the basic concepts of Buddhism and considered the connections between Sila (moral excellence), Samadhi or Bhavana (meditation) and Prajna (wisdom) as connected to mental evolution. She discussed about Buddhist meditative practices of Samatha, Vipasyana and Maithri that are being studied in our department. The principle underlying Buddhist contemplative practices is the notion that 'mind is malleable'. Emotions and mental qualities can be modified and trained just like any other skill. In this respect the Buddhist principles resonate with current cognitive models of Neurosciences and hence with the theme of neuroplasticity. She gave an overview of some of the scientific studies on meditation (there are more than 2500 entries on pubmed and almost 300 studies published in 2012). Generally these studies can be classified based on their effect on neuroplasticity, autonomic function and immune function. She concluded her seminar with a discussion on what meditation is not (it is not just relaxation or an escapism etc). Dr Sajish Chandran successfully defended his PhD work entitled: "Evaluation of autonomic functions and neuroimaging studies in children prenatally exposed to alcohol"
Guide: Dr TN Sathyaprabha (Additional Professor, Neurophysiology) Co-Guide: Dr Pratima Murthy (Professor, Psychiatry) Examiner: Dr KK Deepak, (Professor, Physiology, AIIMS, Delhi) Shivaji Marella (2nd year PhD Scholar) presented his seminar titled "Gut Feelings".
During his talk, Shivaji described how brain and gut maintains a constant and complicated communication which could determine our emotional and even cognitive performance. Some of the interesting points include:
Dr Meghana Kedar defended her PhD work entitled "Characterization of Autonomic Functions in Reflex and Non-Reflex Epilepsy".
Guide: Dr TN Sathyaprabha. Co-Guides: Dr P Satish Chandra, Dr Sanjib Sinha The external examiners - Dr Vengamma (Director-Vice Chancellor Sri Venkatesvara Institute of Medical Sciences, Tirupati) and Dr Anura V Kurpad (Professor of Physiology and Nutrition, St Johns Research Institute and Medical College, Bangalore) were highly appreciative of her work. Dr Shivaji Marella (1st year PhD scholar) presented the paper by Southerland etal from Auton Neurosci.(July 2012) entitled "Activated cranial cervical cord neurons affect left ventricular infarct size and the potential for sudden cardiac death".
Abstract To evaluate whether cervical spinal neurons can influence cardiac indices and myocyte viability in the acutely ischemic heart, the hearts of anesthetized rabbits subjected to 30 min of LAD (left anterior descending) coronary arterial occlusion (CAO) were studied 3h after reperfusion. Control animals were compared to those exposed to pre-emptive high cervical cord stimulation (SCS; the dorsal aspect of the C1-C2 spinal cord was stimulated electrically at 50 Hz; 0.2 ms; 90% of motor threshold, starting 15 min prior to and continuing throughout CAO). Four groups of animals were so tested: 1) neuroaxis intact; 2) prior cervical vagotomy; 3) prior transection of the dorsal spinal columns at C6; and 4) following pharmacological treatment [muscarinic (atropine) or adrenergic (atenolol, prazosin or yohimbine) receptor blockade]. Infarct size (IS) was measured by tetrazolium, expressed as percentage of risk zone. C1-C2 SCS reduced acute ischemia induced IS by 43%, without changing the incidence of sudden cardiac death (SCD). While SCS-induced reduction in IS was unaffected by vagotomy, it was no longer evident following transection of C6 dorsal columns or atropinization. Beta-adrenoceptor blockade eliminated ischemia induced SCD, while alpha-receptor blockade doubled its incidence. During SCS, myocardial ischemia induced SCD was eliminated following vagotomy while remaining unaffected by atropinization. These data indicate that, in contrast to thoracic spinal neurons, i)cranial cervical spinal neurons affect both adrenergic and cholinergic motor outflows to the heart such that ii) their activation modifies ventricular infarctsize and lethal arrhythmogenesis. - - - While presenting the paper, Shivaji added that clinical usage of spinal cord stimulation is on an "intent to treat" basis when the heart is not considered fit for a cardiac procedure (eg - when the arteries are too calcified and a stent cannot be used) and is done via an implantable device post laminectomy at the thoracic level. While this procedure was used as early as 2002, it has not gained much traction. The mechanisms of SCS action in improving heart function has been discussed by Armour etal and Wu etal. Wu etal suggest that the improved cardiac response could be due to regulation of the intrinsic cardiac nervous system (the so called 'brain in the heart' per Armour), redistribution of blood flow, release of catecholamines (via the alpha and beta adrenergic pathways) and the suppression of nociceptive transmission (the severity of pain during a myocardial infarct is in itself is an intense stressor). There was a discussion regarding reperfusion. Here is Shivaji's update, post the journal club: There are many way of looking at what the SCS did in the experiment. The SCS could not have affected perfusion during the actual occlusion period because the artery was mechanically fully closed and the rabbit heart doesn't have collateral circulation. So we can conclude that the effects on actual reperfusion happen post removal of occlusion on the artery. Note that other mechanisms relying on neural mechanisms eg the alpha and beta adrenergic receptor cascades occur during the artery occlusion as well. The other mechanisms which would work during occlusion also include the stabilisation of intrinsic cardiac nervous system. The redistribution of blood flow within the coronary vascular bed has only weak evidence in the literature with contradictory results. Though tissue blood flow in vivo diseased hearts consistently showed such an effect, the in vitro results were not convincing. In a way this shows SCS perhaps works where it counts, ie, in diseased hearts. That blood flow is maintained later is obvious. Once the occlusion is removed the arterial flow is restored. The thing to note here is that the occlusion was acute and reversible. No peripheral vascular bed pathology was present. Ie., once the occlusion was removed, there was no impediment to blood flow. In reperfusion injury to the heart, one of the mechanisms is the larger production of free radical peroxynitrite. This is produced from NO that is locally produced due to a variety of factors. This includes local tissue reflexes and cholinergic innervation. This combines with superoxide released by wbc which come in post reperfusion. (The last paragraph is speculative)The paper showed a balance change in favor of sympathetic system. So the beneficial effect of NO is preserved while reducing the deleterious effects post reperfusion. This could be a way in which reperfusion injury is reduced by SCS. The evidence here is primarily neural, I feel, and their downstream effects on cardiac cells. Far lesser evidence on any vascular mechanisms. Vidyadhara DJ (1st year PhD scholar) presented his first seminar titled "Role of Hypothalamus in Temperature Regulation".
In this wide ranging and yet in-depth physiology seminar, Vidyadhara presented the mechanisms of thermoregulation starting from a historical overview and walk through of Hammel's 1965 set point theory (of the interaction between warm sensitive neurons and temperature insensitive neurons in the anterior hypothalamus/pre-optic nucleus and their influence of warm and cold effectors) and its current revised format and the classic "thermode" studies by Hammel and Benzinger and Nakayama in the 1960's for directly manipulating temperature in the anterior hypothalamus. He discussed thermoregulation via behavioural and autonomic responses; mechanisms of thermogenesis, non thermal factors such as pyrogenic infections, sleep and body temperature; hormonal effects, exercise, dehydration... In closing, Vidyadhara brought up an interesting aspect of thermoregulation at the societal level - asking if global warming and the lack of thermoregulation at that level could make us an endangered species? Dr. Meghana A (3rd year PhD Scholar) presented her seminar on "Neurorehabilitation as a tool to modulate Autonomic function".
Rehabilitation is a process of active change in order to restore the disordered system to optimal function. Meghana spoke about the normal tendency of the body for functional recovery within 6 months and the benefit of providing additional intervention especially for the 25% patients who have moderate to severe disabilities. Recovery strategies include pharmacology, orthopedics, neural stimulation (such as rRTMS and rDCS), neurorehabilitiation etc. Relearning is akin to "teaching new brain old tricks" and neuronal plasticity is a key component to neurorehab. The functional improvement mechanisms could either be recovery or compensation and the neural strategies include resuscitation (natural recovery), recruitment and retraining (compensation). Autonomic function tests are non-invasive and effective diagnostic and prognostic tools. Neurorehabilitation helps in supporting the autonomic nervous system by enhancing the parasympathetic activity. "Effect of a single dose of standard levodopa on cardiac autonomic function in Parkinson's disease" by SJ Sriranjini, Mohan Ganesan, Karuna Datta, Pramod Kumar Pal, Talakad N Sathyaprabha was published in Neurology India. Year : 2011 | Volume : 59 | Issue : 5 | Page : 659-663
ABSTRACT Background: Parkinson's disease (PD) is associated with autonomic dysfunction and chronic levodopa therapy has been reported to impair the autonomic control of heart rate. Aim: Our aim was to assess the immediate effect of a single dose of levodopa on heart rate variability (HRV) in idiopathic PD. Materials and Methods: Eleven patients of idiopathic PD (F:M =2:9, mean age 57.3±8.6 years, duration of illness 4.1±2.8 years, Hoehn and Yahr stage 2.1±0.2) on stable levodopa dosage were studied. Motor part of unified Parkinson's disease rating scale and resting Lead II electrocardiogram (ECG) recordings were performed at baseline (12 hours off medication) and after two tablets of 100/10 mg of standard levodopa/ carbidopa. ECG was recorded continuously in the first hour (H1) followed by a 15-min recording in second (H2), third (H3) and fourth (H4) hours. Artifact free 5-min segments of the ECG were analyzed offline to obtain the HRV parameters in time domain (ms) and frequency domains (ms 2 ). Results: Significant increase was observed in standard deviation of normal to normal intervals (23.5±2.7-46.2±6.6,P<0.05), root mean square of successive differences of NN intervals (16.3±2.9-30.7±5.1, P<0.01), total power (568.9±125.7-2739±667.5, P<0.01), low frequency power (146.5±40.8-614.1±206.7, P<0.05) and high frequency power (107.4±33.9-332.7±85.9, P<0.05) in H1. Conclusion: The results are suggestive of an improvement in the overall variability of the heart rate indicating an enhanced vagal tone. Keywords: Cardiac autonomic dysfunction, levodopa, Parkinson′s disease How to cite the article: Sriranjini SJ, Ganesan M, Datta K, Pal PK, Sathyaprabha TN. Effect of a single dose of standard levodopa on cardiac autonomic function in Parkinson's disease. Neurol India 2011;59:659-63 In today's journal club, Meghana Rao (2nd year PhD scholar) reviewed article from Autonomic Neuroscience entitled Paraventricular nucleus modulates autonomic and neuroendocrine responses to acute restraint stress in rats by Cristiane Busnardo et al.
Takeaways: During stress, GABAergic inhibition causes PVN to be quiescent. At rest, Glutamatergic activation of PVN takes place leading to bradycardia and decreased blood pressure. |
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