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Dr. Suresha Kodapala

Neurologist, Bangalore

550 at clinic
Dr. Suresha Kodapala Neurologist, Bangalore
550 at clinic
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My experience is coupled with genuine concern for my patients. All of my staff is dedicated to your comfort and prompt attention as well....more
My experience is coupled with genuine concern for my patients. All of my staff is dedicated to your comfort and prompt attention as well.
More about Dr. Suresha Kodapala
Dr. Suresha Kodapala is a popular Neurologist in Whitefield, Bangalore. She is currently practising at Telerad RxDx Multispeciality Health Center in Whitefield, Bangalore. Don’t wait in a queue, book an instant appointment online with Dr. Suresha Kodapala on Lybrate.com.

Lybrate.com has a number of highly qualified Neurologists in India. You will find Neurologists with more than 33 years of experience on Lybrate.com. You can find Neurologists online in Bangalore and from across India. View the profile of medical specialists and their reviews from other patients to make an informed decision.

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Telerad RxDx Multispeciality Health Center

Plot No 7g, Opp Graphite India, ITPL Road, Whitefield. Landmark: Next To Maple HotelBangalore Get Directions
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Good Evening Sir, My problem is I am getting shake or vibrations in my hands when I drive any bike for more than 45 mins. Can I know what is the reason?

FRHS, Ph.D Neuro , MPT - Neurology Physiotherapy, D.Sp.Med, DPHM (Health Management ), BPTh/BPT
Physiotherapist, Chennai
It might be of muscle atrophy or of pathological reasons do Take Neuro Conduction Study and do consult Neuro physician and physiotherapist and take appropriate Therapy best wishes.
1 person found this helpful
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I had seizure 3 years ago. I consulted a neurologist and stated taking leviteractam tablets, still taking it. Never had seizure again in 3 years. But I'm unclear about the doctor as he is not commenting on stopping the tablets even after normal EEG reports. What should I do about this?

DM - Neurology, MD - General Medicine, fellowship in interventional neuroradiology
Neurologist, Mumbai
If both neuroimaging and eeg are normal and you never had a seizure in last 3 yrs, your antiepileptic can gradually be withdrawan.
2 people found this helpful
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My wife age 66 yrs having urine incontinence problem too much? her neurosurgery for brain tumor was done in 2007. She also having diabetes. taking treatment at Medicity Gurgaon but no improvement. Did catheretzatiom but she having pain in bladder What should do!

M.S (surgery), M.Ch - Neuro Surgery
Neurosurgeon, Gurgaon
Other alternative treatment urinary incontinence is pacemaker but it can be considered only if life expectancy after tumor surgery is good.
1 person found this helpful

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.

3 people found this helpful

I am a 43 years old man. I am suffering from depression and migrain pain from 8 years. I could not concentrate som time. Please Advice me.

M.D,Psychiatry
Psychiatrist, Amritsar
If your diagnosis is made by psychiatrist then start tab sodium valproate 500mg at night, tab headset sos and take tab dulouxetine 20mgdaily. Report after 10 days.
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Hi I am 17 years old I have this problem that sometimes my hands begin to shake unnecessarily. Please help me with a cure. Thank you.

B.Sc. - Dietitics / Nutrition, Nutrition Certification,Registered Dietitian
Dietitian/Nutritionist, Delhi
1. Keep yourself hydrated. 2. Get extra rest for some days till you feel more energetic. 3. Avoid watching television for long hours. Indulge in relaxing activities. 4. Avoid stress and too much physical exertion. 5. Take a nutritious diet with more protein items in homemade food like soya, sprouts, dals, paneer, milk, seasonal fruits. 6. Do light physical activity, meditation and yoga. 7. Take one good multivitamin tablet after food for 7 days.
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Hi! Im 26years. I have a shivering problem. My hands shake at times even I have healthy food. Cloud please suggest me any home remedy. Thanks.

MBBS
General Physician, Cuttack
. 1. It could be due to essential tremor. The cause of the tremor is unknown. In some cases it is hereditary and runs in families. There is no definite treatment unless it is severe 2 other causes of tremor could be stress, anxiety, panic, nervousness, inadequate sleep, physical exhaustion, strong emotion, hyperthyroidism, hypoglycemia, smoking/tobacco/alcohol abuse/withdrawl, excess tea/coffee, drugs like steroid/amphetamine, neurological disorder, 3. Investigate yourself to exclude the above causes of tremor after consulting neurologist 4. Avoid stress/anxiety/nervousness/ panic etc 5. Avoid excess tea/coffee/ smoking/alcohol 6. Take good nourishing diet 7. Have adequate sleep. 8. Do a thyroid function test to exclude thyroid problem 9. Consult neurologist for further advice.
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My father in law who is 61 yrs now had undergone angioplasty in 2007. The stent was inserted through the right side. From last year there is numbness (less sensation) on the right thigh and pain occurs when he stands for a long time or walks for about 2 kms. Is it due to the operation or some other cause? kindly advice.

B.H.M.S., Senior Homeopath Consultant
Homeopath, Delhi
Dr. Reckeweg's r - 3 and Dr. Reckeweg's r - 63 / 10 - 10 drops in little water thrice a day for one month. Keep a 10 to 15 minutes gap in between these medicines. Revert back after one month with feedback.
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I have migraine what should do for its permanent solution pls tell me during headache I feel vomiting and acidity too.

MBBS
General Physician, Madhubani
The most important factor for migraine is triggering factor. It might be anything from acidity, smell of masala, too hot or too cold. Try to avoid it. Change your lifestyle. Wake up early in the morning. Walk on grass bare foot in early morning. Yoga. Don't remain empty stomach for long period. Migraine is precipitated by menstruation. Avoid all these. There is no permanent cure of migraine. Whenever you have attack of migraine just go to cool calm dark place. Take a nap of half an hour. Use tab Headset half tab on acute attack. Use tab pan-d to prevent vomiting and acidity.
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Dear sir, I am suffering from insomnia for last few weeks. Whenever try to sleeping, it rakes couple of hours to go into sleep. Sir please provide me some tips to overcome this problem.

PDDM, MHA, MBBS
General Physician, Nashik
1. Avoid caffeine found in coffee, tea, chocolate, cola, and some pain relievers.[four to six hours before bedtime.] 2. Quiet, dark, and cool environment can help promote sound sleep. [use heavy curtains, or an eye mask to block light, and also keeping computers, tvs, and other work materials out of the room will help promote mental bonding between your bedroom and sleep] 3. Avoid stressful, stimulating activities like doing work, discussing emotional issues. Physically and psychologically stressful activities can cause the body to secrete the stress hormone cortisol, which is associated with increasing alertness.
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I am 60 years, diabetic for five years, on Metaforte-500mg, 1-0-1, I do pranayama, sudarshan Kriya yoga, morning my breakfast will be invariably protein shake (herbalife) and my sugar is under control (98 -110) fasting and 140-150 PPBS. HBA1c is 6.5. My problem is foot neuropathy, there is no total numbness, but lot of talking and burning sensation. My doctor says HBA1c should be brought down to 6. My BP will vary from 135/90 to 140/95. Please suggest some remedy for foot neuropathy.

BSc Home Science, M.Sc - Dietitics / Nutrition
Dietitian/Nutritionist, Bangalore
Vitamin b will definitely help in food neuropathy. Are you a member of herbal life? with diabetes you have to take more fibre, protein, variety of veg, 3-4 fruit servings in a day but in moderate amounts because of diabetes, very sweet fruits like banana, mango, sitaphal, cheeku etc are restricted. Eat dry fruits especially wall nuts & flex seeds for omega 3 & sprouts for fibre etc. In diabetes there are multiple nutrient deficiencies and food cravings. To correct them and feel better, you must take some dietary supplements as diabetic people have more nutritional needs. For in-depth understanding, planning optimum diet to deal with deficiencies & other concerns with weight gain
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My son after epilepsy got over, now facing(past 5 yrs) Hearing hallucination.He is 31 yrs.& taking Halo Piridol 1.5 mg 0-0-2, Clozopine 100 mg 0-0-1, Dichorate 250 mg 0-0-1, Mirt 15 mg 0-0-1,D-vinit 0-0-1, Topirol 50 mg 0-0-1, THL(pacitane) 0-0-1, Hearing is not violent now; but occasionally he gets suicide tendency. Is there any way out. For this ?

Hypnotherapist, DCS, BSIC, Advanced Trainee of Transactional Analysis, Advanced Skills in Counselling
Psychologist,
Ayurveda system has excellent treatment for this type of illness. Let him also meet a counsellor to overcome suicide thoughts.
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I am feeling uneasy in my left hand finger. I am not getting pain but its like its getting numb. Finger is working but still feel like numb on it.

Neurologist,
If your symptoms had been in the The first three digits of a hand, it could be carpal tunnel syndrome- a pinched nerve in your wrist. If the symptoms are in last 2 digits of the hand, it could a different type of pinched nerve. If numbness and tingling is in whole hand- it could be neuropathy. If numbness in fingers is associated with neck pain and radiating pain in arm- it could be a pinched nerve in your cervical spine. So based on the information you share, it is hard to draw any conclusions about what you have.
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I really need some advice or more better if help. Symptoms - fat deposition on my chest, waist, hips. Nipples look swollen up when body temp. Is hot and shrinks to normal when come in touch to cold things or in cold environment. It is happening from the time I ran into puberty but fat deposition started 2 years ago. But now its embarrassing. I use to have medical history of seizure disorder and its medication course was completed a year ago. Some thing I did't added previously. Doctors gave me sodium valporate 600 mg everyday. But due to overdose I got acute pancreatitis then they switch me to sodium dilantin 300 mg/day at night. This case is 6 year old. At that time it started. I consulted the doctor he said it will go away with time but it did not instead it increased but slowly. G - male Age - 20.

MBBS, MD Psychiatry, DNB Psychiatry
Psychiatrist, Nagpur
Fat deposition in breasts in men is a reported side effect, though rare, with some medications, which include phenytoin sodium. Weight gain in general is seen as a side effect with sodium valproate too. Anticonvulsants like phenytoin may at times cause alterations in male hormone levels too, that is the most probable explaination for your symptoms. Consult your treating physician and a endocrinologist if possible to get a thorough evaluation. The commonest explaination could be also as simple as being overweight.
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Mere father ka recently operation hua hai brain ka unke brain me blood clotting ho gyi thi kal hi vo discharge hoke aaye hai hospital se unke stitches lagge hua hai dressing hai but Bhi vo gussa bahut karne lagge sir PE bahut pressure daal k chillane lage to unke aakh k upar swelling ho gyi hai to me kya karu ab I mean koi serious dikkat hai?

MS - General Surgery, DNB - Neuro Surgery
Neurosurgeon, Vadodara
Mild swelling post operative over forehead and eyes is normal. That will resolve over few days. Do not worry about that. And about his behavior, there are some changes in behavior after brain injury especially in case of frontal lobe. So give him some time. All will settle with time.
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Could you suggest some medicine for migraine please. I am feeling very pain in my left frontal lobe of my head. Some time it is very high.

MBBS, MD - Internal Medicine
Internal Medicine Specialist, Faridabad
Hello... take tab. vasograine for pain of migraine. To make better immunity take Powder protinex 1 tsf with milk once a day after meal. there many causes of headache i.e. eye disease or vision problems, stress, fever, high B.P. , acidity, injury, migraine, incomplete sleep, cervical pain, constipation, pl. checkup your B.P. blood sugar level, cbc, after tests consult again. Avoid stress, avoid fatty meal, oily foods , take lemon tea, take protein diet or amino acid diets, take good sleep at night, take green veg., plenty of water. Juice, Welcome in lybrate .
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My age is 23. Height 6ft weight 78 kg. I am having bone pain. Numbness and tingling of whole body legs and feet and inflammation. Today I had fasting blood test which came calcium 9.7 vitamin d3 113 alkaline phosphate 56 Phosphorus 3.3 ldh 152. I was suspected of cancer because bone pain increasing day by day. Does ldh 152 indicate that I do not have cancer.

PG Diploma in Emergency Medicine Services (PGDEMS), Bachelor of Ayurveda, Medicine and Surgery (BAMS), MD - Alternate Medicine
Ayurveda, Ghaziabad
Hi Apply pranacharya restopain oil or prasarini oil on your affected part then give hot fomentation. Take maha rasnadi kwath 2-2 tsf twice a day. And agni tundi vati and maha yograj guggul 1-1 tab twice a day..
1 person found this helpful
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I have headache. What I should do? I occurs frequently. What are the symptoms of migraine?

MBBS
General Physician, Cuttack
Take one tablet of crocin 500mg sos after food, drink plenty of water and take rest. If it is a chronic headache it could be due to anxiety,stress,depression or migraine. Avoid stress.Check your Bp,eye sight and rule out sinusitis.Consult neurologist if you have recurrent headache .The symptoms of migraine are Unilateral throbbing and pulsating headache ,eye pain,nausea,vomiting,increased sensitivity to light and sound,feeling of dizzy or faintness
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My hand shivers all the time and it become tremendous when I got nervous, though I am only 22 years old. Is there any remedy to cure it?

MBBS
General Physician, Jalgaon
Please Consult nearby neurologist Get investigated and take proper treatment Meanwhile Wake up early go for morning walk in greenery daily Do yogasanas and pranayam daily Do meditation regularly Take Saraswatarishta 15 ml twice daily with water.
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