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Dr. Mangesh

Neurologist, Pune

700 at clinic
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Dr. Mangesh Neurologist, Pune
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Our team includes experienced and caring professionals who share the belief that our care should be comprehensive and courteous - responding fully to your individual needs and preferences....more
Our team includes experienced and caring professionals who share the belief that our care should be comprehensive and courteous - responding fully to your individual needs and preferences.
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Dr. Mangesh is a renowned Neurologist in Karve Road, Pune. You can visit him/her at Sahydree Hospital in Karve Road, Pune. Don’t wait in a queue, book an instant appointment online with Dr. Mangesh on Lybrate.com.

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39/25 Shankar Smruti Kachare Wadiln 9, Karve Road Deccan, PunePune Get Directions
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I am 66 years old lady and had undergone knee replacement surgery one year back .Some times gets the. Pain due to cervical spontelasys . Little over weight . I am having issues of numbness in my fingers and legs at times ,especially from sleeping positions .

M.B.,B.S., Post-Graduate (Aviation, Sports & Internal Medicine), PhD - Holistic Medicine, DHA, DAc, MD - Acupuncture, CHt
Alternative Medicine Specialist, Delhi
I am 66 years old lady and had undergone knee replacement surgery one year back .Some times gets the. Pain due to cer...
You appear to suffer from degenerative {premature aging} damage to your spine, as in your knees and peripheral neuropathy - need investigations to establish diagnosis- these problems are chronic and progressive. Conventional medicine does not usually offer any definitive arrest or reversal of such ailments. However, for good results I recommend holistic medicine therapy to you.
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I am 35 years old female. I have migraine for last 22 years. It's affecting my day to day life. Earlier it used be only headache. Now I get headache, eye pain, numbness in arms n legs, also I see sm image in front of my eye like a thin horizontal line. Headache happens after every 5 or 6 days. Donot get relief with pain killers also. No vomiting but spinning of head is there. Can't bear loud music, sunlight and also travelling has become difficult. Its a throbbing pounding pain on one side n sometimes near the ear. Please suggest medicine.

MBBS
General Physician, Cuttack
1.Take Paracetamol 500mg one Tablet sos after food up to a maximum of three tablets daily at the time of attack 2.Drink plenty of water and take rest. 3.. Avoid stress, anxiety, depression, agitation,exposure to loud noise, bright light since it precipitates migraine attack 4.. Go for regular exercise 5. practice yoga, meditation, deep breathing exercise to calm your mind, control your emotion and relieve you from stress 6. If You have chronic migraine, you have to take migraine prophylaxis after consulting physician
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My bro got epilepsy attack in morning n again now inspite of regular medication with zefretol, lamitor DT, and levipil. He has fever also. What to do now? No doctors are available today.

MBBS, Diploma in Nutrition and Health Education (DNHE), Diploma in Clinical Cosmetology
General Physician, Noida
My bro got epilepsy attack in morning n again now inspite of regular medication with zefretol, lamitor DT, and levipi...
CT scan/ EEG was done? can cause of seizure was detected ? I want to tell you that medicine as advised by your Doctor need to be taken regularly and must not missed dose even for single day You can Consult Good Neurologist for second opinion, i can guide you further
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I am 30 years old girl, I am suffering from parkinson from last 20 years whenever I do yoga n stretching exercises I had pain in my spinal cord and back pain, what all this sign mean.

MD - Homeopathy, BHMS
Homeopath, Vadodara
I am 30 years old girl, I am suffering from parkinson from last 20 years whenever I do yoga n stretching exercises I ...
As you already are suffering from severe disease this can be the symptoms of the same. Parkinson's is rare in young age, I would like to see your report and than only can advise you or help you. You can consult me through Lybrate for Homoeopathic treatment and further guidance.
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Hello Dr. am 27years old weight around 72 kg around 20 days before diagnosed hypothyroidism value is 7.65. I hv started medicine from d day starting I thought am feeling Ms. pain in lower part of legs, insomnia problem or yesterday I feel unconsciousness also. Sumtyms nauseating. Is it du E to medicine. Taking eltroxin 25 mg.

D.A.M.S( A. M.), D.AC/B.E.M.S
Acupressurist, Mumbai
Hello Dr. am 27years old weight around 72 kg around 20 days before diagnosed hypothyroidism value is 7.65. I hv start...
You should take acupressure treatment and try take Biochemic ferrum phos3x+ calc flour 3x. 4 tab each thrice a day with warm water.takes it.5days & consult me private online.
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Parkinson s Disease

MBBS, DNB, Fellowship In Neurosurgery
Neurosurgeon, Kolkata
Parkinson s Disease

Deep brain stimulation in Parkinson’s disease

Abstract: Deep brain stimulation (DBS) is a widely accepted therapy for medically refractory Parkinson’s disease (PD). Both globus pallidus internus (GPi) and subthalamic nucleus (STN) stimulation are safe and effective in improving the symptoms of PD and reducing dyskinesias. STN DBS is the most commonly performed surgery for PD as compared to GPi DBS. Ventral intermediate nucleus (Vim) DBS is infrequently used as an alternative for tremor predominant PD patients.

Patient selection is critical in achieving good outcomes. Differential diagnosis should be emphasized as well as neurological and nonneurological comorbidities. Good response to a levodopa challenge is an important predictor of favorable long-term outcomes. The DBS surgery is typically performed in an awake patient and involves stereotactic frame application, CT/MRI imaging, anatomical targeting, physiological confirmation, and implantation of the DBS lead and pulse generator. Anatomical targeting consists of direct visualization of the target in MR images, formula-derived coordinates based on the anterior and posterior commissures, and reformatted anatomical stereotactic atlases. Physiological verification is achieved most commonly via microelectrode recording followed by implantation of the DBS lead and intraoperative test stimulation to assess benefits and side effects. The various aspects of DBS surgery will be discussed.

Key words: deep brain stimulation (DBS); Parkinson’s disease(PD),  stereotaxis

Introduction

Parkinson's disease is a slowly progressive, neurodegenerative disease characterized by tremor, rigidity, bradykinesia and postural instability. It is the most common movement disorder in middle or late life with a prevalence of about 0.3% of the general population, rising to 1% in people over 60 years of age. Approximately 130 000 people suffer from it in the UK and it presents an increasing burden in our ageing population. Pathological findings in Parkinson's disease demonstrate greatly diminished neuromelanin pigmented neurons in the substantia nigra of the basal ganglia with associated gliosis, and Lewy bodies present in many remaining neurons.

James Parkinson, in his original 1817 Essay on The Shaking Palsy, gave an account of six patients in which he noted signs of tremor, festinating gait and flexed posture.  Nearly two centuries from Parkinson's observations, and almost four decades after Cotzias' dramatic demonstration of levodopa's efficacy, the limitations and complications of levodopa treatment for Parkinson's disease have become well documented Five years after initiation of therapy, a majority of patients develop medication related motor complications, namely levodopa induced dyskinesias (LID) and motor fluctuations. Deep brain stimulation (DBS) has been developed primarily to address these treatment related motor complications and therapeutic failures.

Pathophysiology of PD

The loss of dopaminergic neurons in the substantia nigra, the main functional characteristic of PD, affects the circuit described above and leads to the cardinal motor symptoms of PD. While the exact mechanism of this process is unknown, animal research as well as human recordings have provided functional and biochemical evidence that bradykinesia in PD results from excessive activity in the STN and the GPi. This leads to an exaggerated beta (10-30 Hz) synchronization within and between structures in the basal ganglia circuitry  that could also contribute to rigidity and akinesia.

The pathophysiology of rest tremor in PD is less clear and probably more complicated. This symptom most likely results from a dysfunction of both the striato-pallidal-thalamocortical and the cerebellodentato-thalamocortical circuits, with hyperactivity and hypersynchronization between central oscillators.

Possible mechanism of action of DBS

DBS acts through delivering an electrical current in a specific target area of the brain. This current can be modulated through modification of voltage, frequency and duration of each electrical pulse delivered. The delivered energy creates an electrical field of variable size and shape according to the parameters used for stimulation. Although initially believed to stimulate the target, thus the name of the whole process, it seems that

DBS actually excites the neuronal fibers, but inhibits the neural cells. In fact, GPi DBS decreases the GPi mean firing rate back to a normal range in animal models as well as PD patients, and high frequency DBS has a similar effect as dopamine replacement therapies, and promotes faster (about 70 Hz) nonhypersynchronous activity in the basal ganglia, correlated with clinical improvement. This might be achieved through stimulation of bypassing inhibitory pathways, synaptic inhibition, depolarizing blockade, synaptic depression, and simulation-induced disruption of pathological network activity. Overall, this leads to modifications of the firing rate and pattern of neurons in the basal ganglia, as well as local release of neurotransmitters such as glutamate and adenosine. In addition, it seems that DBS also increases blood flow and stimulates neurogenesis. Over the last few years, functional imaging, specifically functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and single-photon emission computed tomography (SPECT), has been used in an attempt to clarify the mechanism of action of DBS. In fMRI, blood-oxygen-level-dependent (BOLD) signals are acquired, and oxygenated blood marks areas of neural stimulation or inhibition. On the other hand, PET and SPECT allow for imaging of multiple activity markers, such as blood flow, glucose and oxygen metabolism. While fMRI is less powerful than nuclear medicine techniques, it provides a much better spatial and temporal resolution. Because of the suspected inhibitory DBS effects in electrophysiological studies, reduced STN blood flow or glucose metabolism would have been expected on functional imaging. However, the opposite has been found to be true in an overwhelming majority of imaging studies to date. In addition, BOLD activation in the area surrounding the electrode has been reported, despite the electrode imaging artifact preventing direct observation of the STN around the electrode. This discrepancy between apparent STN inhibition in single-cell studies and activation in imaging studies might be explained by a few hypotheses. First, electrophysiological recordings identify short neuronal modulation (in the order of milliseconds) while neuroimaging methods may reflect the summed activity changes over seconds to minutes. Second, non-neuronal contributions to the change in blood flow and/or glucose metabolism cannot be excluded, and could confound the results of neuroimaging.

Finally, it is possible that PET and fMRI actually detect the increased activity in the axons, rather than in the cell bodies. Complicating matters further, some imaging studies after STN DBS have showed increased

activity in the GPi while others reported decreased activity in that nucleus. In summary, it is still unclear how exactly DBS affects the firing rate and pattern of neurons and how these changes actually modify the symptoms of Parkinson’s disease. DBS is presently more of an empirically proven treatment in search of physiological explanation.

The effect of DBS on the cardinal symptoms of PD have been established in three randomized controlled clinical trials --- 

TABLE 1

Author, year

 

No of patients

Follow up

Target

Results

Deuschl et al., 2006

156

6 months

BL STN

QOL better with DBS, motor symptom better with DBS

 

Weaver et al., 2009

255

6 months

BL STN or GPi

Dyskinesia free ON time better with DBS

 

Williams et al., 2010

366

12 months

BL STN  or GPi

QOL better with DBS

 

 

PATIENT SELECTION for DBS in PD

Patient selection is a critical first step as poorly chosen candidates may not have optimal benefits and have increased morbidity. Several factors must be considered before determining if a patient is an appropriate candidate for DBS surgery. A multidisciplinary approach involving the neurosurgeon, neurologist, and neuropsychologist is important to determine the appropriate surgical candidate. It is also important that the diagnosis of idiopathic PD be confirmed prior to proceeding with DBS surgery. Key to this assessment is evaluating the surgical candidate in both the on and off medication states with a corroborating levodopa challenge. Perhaps the best prognostic indicator of a patient’s suitability for DBS surgery is their response to levodopa.In general, a levodopa challenge following a 12-hour medication withdrawal should provide at least a 33% improvement in the motor section of the Unified Parkinson’s Disease Rating Scale (UPDRS).

                     In our institute, we follow a simple chart(below) for screening of patients for DBS in PD.

 

 

  1.  

Age<75 years

 

  •  

No

  1.  

Idiopathic PD ( No PSP/MSA/NSD etc)

 

  •  

No

  1.  

Levodopa responsive  

                      

  •  

No

  1.  

Poor/adverse response to drug          

 

  1.  Increased off period                                                              

 

  1. Disabling dyskinesia                                                              

 

 

  1. Disabling motor fluctuations                 

 

 

Yes

 

Yes

 

 

Yes

 

 

No

 

No

 

 

No

  1.  

Degree of disability(UPDRS part III score)>25

 

  •  

No

  1.  

Neuropsychology, MMSE>24

 

  •  

No

  1.  

LEVODOPA CHALLENGE RESPONSE POSITIVE                                                   

 

(30% improvement in UPDRS after 12-hours off medication)

 

  •  

No

  1.  

Advanced  co-morbidity

 

Yes

  •  
  1.  

long term anticoagulation

 

Yes

  •  
  1.  

Willing for surgery and programming

 

  •  

No

 

 

PREOPERATIVE MANAGEMENT

A full medical assessment is a necessary part of the preoperative evaluation, as advanced PD patients tend to be elderly with significant comorbidities. Major issues are---

 

Anticoagulation/antiplatelets--- The risk of discontinuing medications that affect anticoagulation and

platelet aggregation should be weighed against the potential benefits in the quality of life offered by DBS surgery. However, timely discontinuation of these latter medications is mandatory for stereotactic surgery since intracerebral hematomas are the most serious of all potential complications from DBS. Any anticlotting medications, including aspirin, ticlopidine, clopidogrel, and all nonsteroidal anti-inflammatory drugs should be discontinued at least 7 to 10 days preoperatively to ensure the return of normal blood clotting function.

Arterial hypertension can also increase the risk of intracranial bleeding during stereotactic procedures and must be controlled in the weeks prior to surgery.

A prolonged discussion on the short- and long-term effects of DBS on Parkinson’s disease should be carried out with the patient, family, and caregivers.

The night prior to DBS surgery, the antiparkinsonian medications are typically held to pronounce the Parkinson’s symptoms at the time of surgery to see the clinical effects on symptoms during surgery and the families must be counselled regarding their role in facilitating the patient.

Target selection

The two main targets considered for DBS in PD are the STN and the GPi. current tendency is to prefer targeting the STN because of a greater improvement in the OFF phase motor symptoms as well as a higher chance to decrease the medication dosage and a lower battery consumption linked to the use of lower voltage in the STN compared to the GPi DBS. GPi can be the preferred target if LID is the main complaint. GPi DBS might be preferred for patients with mild cognitive impairment and psychiatric symptoms. Because STN DBS might have a higher rate of cognitive decline and/or depression and worsening of verbal fluency in some studies.

Surgical technique

The basic components of DBS implantation surgery involve frame placement, anatomical targeting, physiological mapping, evaluation of macrostimulation thresholds for improvement in motor symptoms or induction of side effects, implantation of the DBS electrode and implantable pulse generator (IPG).

Head-frame placement

The CRW frame is the most commonly used followed by the Leksell frame. Placement of the frame is done under local anesthesia unless anxiety or uncontrollable movements necessitate the use of sedation or general anesthesia.

Leksell stereotactic frame  placed over the head of a patient showing the correct method for placement of the Leksell head-frame. The frame should be placed parallel to orbito-meatal line in order to approximate the AC-PC plane. It is attached to the patient’s head using four pins under local anesthesia.

Imaging and anatomic targeting

Computerized Tomography (CT) scans and MRI are the two main imaging modalities used for targeting when performing DBS implantations. A thin cut stereotactic CT (_2 mm slices with no gap and no gantry tilt) is obtained after frame placement and is then fused with the stereotactic MRI on a planning station (Stealth station). The advantage of fusing the CT with MRI is the ability to avoid image-distortions inherent to MR imaging adding to the stereotactic accuracy. To better define the STN, T2-weighted images (TR 2800, TE 90, flip angle 90˚, slice thickness 2.0 mm) were obtained.

The AC and the PC were marked and the centre of the AC–PC line determined. The next step is planning the entry point and trajectory. The strategy here is to avoid surface and sub-cortical vessels. After trajectory planning, the patient is placed supine on the operating table and the frame attached to the table using an adaptor. Prophylactic antibiotics are given at least 30 min prior to incision. The head is prepped and draped in a sterile fashion. Under local anesthesia, a burr-hole is placed on the calculated entry point marked on the skull. The entry point is determined by the calculated arc and ring angles. Hemostasis is achieved with bone wax and bipolar cautery.

A Medronic Stim-Loc anchoring device (Medtronic, Minneapolis, MN) burr-hole base ring is then placed on the burr-hole and secured with two screws which are used at the end of the procedure to anchor the DBS electrode.

The dura is then cauterized and opened exposing the underlying surface of the brain. The microdrive is then assembled and cannulae inserted 10 mm above the target to avoid lenticulostriate vessels found deeper. Gel- foam and fibrin glue is applied on dural hole to minimize cerebrospinal fluid (CSF) loss and air entry into the skull. Subsequently, microelectrode recording and stimulation is undertaken.

Microelectrode recording/ Mapping

Microelectrode mapping is used to precisely define the target STN and its boundaries as well as nearby critical structures. We believe microelectrode mapping is crucial in order to give one the best chance for optimal placement of the DBS lead given anatomical inaccuracies due to image distortion and intraoperative brain shifts secondary to CSF loss, and pneumocephalus that can lead to inaccuracies in defining the initial target coordinates and shifts in the target itself once the skull is opened. Microelectrode mapping is performed using platinum-iridium glass coated microelectrodes dipped in platinum black with an impedance of around 0.3–0.5 Mo. These platinum-iridium microelectrodes are capable of recording single unit activity and can also be used for micro-stimulation up to 100 mAwithout significant breakdown in their recording qualities.

As the recording electrode was advanced, entry into the STN was identified by a sudden increase in the density of cellular discharge, with the characteristic irregular pattern of discharge—spikes of different sizes, occurring at random intervals. On coming out of the STN a quiet period (background noise) was seen followed by recording from the substantia nigra if the recording was continued far enough, described as high frequency (50–60 spikes/s) discharge pattern.11 Characteristic STN recordings (visual and audio) were identified and the depth of the STN activity was noted. Identification of STN activity was only based on the visual identification. The centre of the point of best electrical activity was selected as the final target. The microelectrode was replaced with a permanent quadripolar macroelectrode (Medtronic electrode no. 3389) to target the centre of the STN electrical activity. The proximal part of this electrode consists of four nickel conductor wires insulated with a polytetrafluoroethylene jacket tubing. The distal part has four metallic noninsulated contacts of 1.5 mm spaced at 0.5 mm intervals. The diameter of the distal electrode is 1.27 mm. Based on the clinical response any of the four contacts can be used for stimulation. Macrostimulation using the DBS electrode itself is then used to determine benefits and side effects. In most cases lateral skull x rays were obtained at this point with image intensifier carefully positioned to locate the target point in the centre of the Leksell-G frame rings.

Initial programming is always refined by using intra-operative macrostimulation data and a mono-polar review to identify the thresholds of stimulation for improvement in parkinsonian motor signs as well as the thresholds for inducing side effects at the level of each contact. The four variables that are used in programming are choice of contacts (0, 1, 2 or 3 used either as the cathode or anode), frequency of stimulation (hertz), pulse-width (ms) and amplitude (voltage).

POSTOPERATIVE MANAGEMENT

In the immediate hours after surgery, it is important to keep arterial blood pressure in the normal range. In addition, the patient’s preoperative drug regimen should be restarted immediately after surgery to avoid problems with dopaminergic withdrawal. Patients should undergo postoperative CT scans and/or MRI scans to assess the electrode location and intracranial status. In addition, plain X-rays are obtained to assess the location and geometry of the leads and hardware. Parkinson’s medications may need to be adjusted depending on the patient’s status. Cognitive and behavioral changes may occur in the postoperative period, particularly in older patients. Patients can be discharged as early as 24 hours after surgery, depending on their neurological and cognitive status.

Conclusion

For the last 50 years, levodopa has been the cornerstone of PD management. However, a majority of patients develop motor fluctuations and/or LID about 5 years after the initiation of therapy. DBS of the STN or the GPI grant to patients with PD improved quality of life and decreased motor complications, and has been approved as such by the Food and Drug Administration in the US in 2002. We reviewed the experience and available literature on DBS for Parkinson’s disease over the last decade and arrive at the following understandings.

The success of DBS surgery depends on the accurate placement of the leads and meticulous programming of the stimulation. Therefore, it is best accomplished by an experienced team of neurosurgeon, neurologist, and support staff dedicated to the treatment.

Reports of surgical complication rates and long-term side-effects of DBS are very variable, so benefits and potential adverse results should not be under- or over-emphasized.

While essentially equal in improving the motor symptoms of PD, STN and GPi might have their own benefits and risks, and the choice of the target should be individualized and adapted to the patient’s situation.

Knowledge to further improve DBS treatment for Parkinson’s disease, such as a more scientific and reliable protocol on programming, strategies to minimize cognitive and psychiatric complications, and the better

long-term maintenance of the implanted device, are still lacking.

Data on the impact of DBS on non-motor symptoms affecting the quality of life of PD patients, such as pain, speech or gastro-intestinal complaints, are still scarce. Further research in these areas will help make this useful treatment even more beneficial.

4 people found this helpful

I am a migraine patient. Can you suggest me what I can do to prevent headache in sunlight?

PGDHHM, MBBS
General Physician, Delhi
Exposure to the sunlight can trigger headache in some. Best way is to wear sunglasses to avoid direct exposure to sunlight. Drink plenty of liquids to maintain hydration. Hope this helps u.
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I want homeopathy medicine for insomnia; 75; no tv/no reading/no worries/no depression/no thoughts after 10pm; I just dont get sleep even though I lie on bed; for sleeping soundly for 6-8 hrs, please suggest strong homeopathy medicine;

BHMS
Homeopath, Faridabad
I want homeopathy medicine for insomnia; 75; no tv/no
reading/no worries/no depression/no thoughts after 10pm; I just...
Hi, there are two types of insomnia: primary insomnia and secondary insomnia. Primary insomnia: primary insomnia means that a person is having sleep problems that are not directly associated with any other health condition or problem. Secondary insomnia: secondary insomnia means that a person is having sleep problems because of something else, such as a health condition (like asthma, depression, arthritis, cancer, or heartburn); pain; medication they are taking; or a substance they are using (like alcohol). Sleep plays a vital role in good health and well-being throughout your life. Getting enough quality sleep at the right times can help protect your mental health, physical health, quality of life, and safety. In children and teens, sleep also helps support growth and development. The damage from sleep deficiency can occur in an instant (such as a car crash), or it can harm you over time. For example, ongoing sleep deficiency can raise your risk for some chronic health problems. It also can affect how well you think, react, work, learn, and get along with others. Management: here are five tips everyone can use to help improve the quality of their sleep: keep your bedroom cool and dark put away/turn off all electronic devices while preparing for bedtime stick to a regular bedtime and wake time every day, even on weekends stop drinking caffeine by the early afternoon and avoid large late-night meals skip the late-afternoon nap, as it can make it harder to sleep at bedtime avoid taking unnecessary stress/ tension. Do regular exercise. Go for a brisk walk in the morning. Medication: take schwabe's bacopa monierri 1x/ thrice daily and kali phos./ once daily at night for 1 month.
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