Common Specialities
{{speciality.keyWord}}
Common Issues
{{issue.keyWord}}
Common Treatments
{{treatment.keyWord}}
Book
Call

Dr. Balaji Pai

Neurologist, Bangalore

400 at clinic
Book Appointment
Call Doctor
Dr. Balaji Pai Neurologist, Bangalore
400 at clinic
Book Appointment
Call Doctor
Submit Feedback
Report Issue
Get Help
Feed
Services

Personal Statement

To provide my patients with the highest quality healthcare, I'm dedicated to the newest advancements and keep up-to-date with the latest health care technologies....more
To provide my patients with the highest quality healthcare, I'm dedicated to the newest advancements and keep up-to-date with the latest health care technologies.
More about Dr. Balaji Pai
Dr. Balaji Pai is a renowned Neurologist in Race Course Road, Bangalore. You can visit him at Mallige Medical Centre in Race Course Road, Bangalore. You can book an instant appointment online with Dr. Balaji Pai on Lybrate.com.

Find numerous Neurologists in India from the comfort of your home on Lybrate.com. You will find Neurologists with more than 42 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.

Info

Languages spoken
English
Professional Memberships
Indian Medical Association (IMA)

Location

Book Clinic Appointment

Mallige Medical Centre

#31/32, Crescent Road, Near Race course Road & Shivananda Circle, Gandhinagar. Landmark: Opp. to Hotel Bangalore InternationalBangalore Get Directions
400 at clinic
...more
View All

Services

View All Services

Submit Feedback

Submit a review for Dr. Balaji Pai

Your feedback matters!
Write a Review

Feed

Nothing posted by this doctor yet. Here are some posts by similar doctors.

I am 39 years old, I have two problem since childhood one is migraine and second is pain in right leg.

MBBS, cc USG
General Physician, Gurgaon
I am 39 years old, I have two problem since childhood one is migraine and second is pain in right leg.
I am giving some health tips for Migraine headache ?1.You can turn off light for some time ?2.Apply hot or cold compresses to your head or neck. ?Ice packs have a numbing effect, which may dull the sensation of pain. ?Hot packs and heating pads can relax tense muscles. ? ?3.Warm showers or baths may have a similar effect. ?4.You can take Tea or coffee( but not excess) 5.Sleep well Here are some tips to encourage sound sleep. Establish regular sleep hours. ?Minimize distractions. ?Your eating habits can influence your migraines. ?Be consistent. Eat at about the same time every day. Don't skip meals. Fasting increases the risk of migraines Avoid foods that trigger migraines kindly consult Physician for further management LEG PAIN: 1.You can take Tablet Paracetamol 500 mg one tablet stat after food 2.You Can do Hot fomentation twice a day for 3 days I am giving to some common reasons for LEG PAIN 1. generalized weakness 2. Anaemia 3. physical exertion and any Trauma 4. lack of protein in Diet 5. any infection present on leg or foot 6. muscle weakness 7 abrupt start/ stop of physical exercise 8. Vit D and Calcium Deficiency
1 person found this helpful
Submit FeedbackFeedback
Submit FeedbackFeedback

What are the symptoms of a migraine headache and what causes migraine as she is having headache from past few days.

BAMS
Ayurveda, Bangalore
HI, The symptoms of migraine are constant headache either partial or complete associated with vomitting, eye pain, irritable mood, nausea and loss of appetite. Migrane is caused due to the vasoconstriction of the vessels of the head or forehead.
Submit FeedbackFeedback

I hv migraine head achr. How to stop dis. Suffering heavily. I can not see movies, reading books, papers etc etc. please help me anyone.

MBBS
General Physician, Mumbai
Migrane- It is characterised by one sided headache which is pulsatile in nature and with a throbbing pain usually with an aura and we can start with tablet propranolol after personal examination
Submit FeedbackFeedback

My mom suffered from bell's palsy but now she has almost recovered. Can she take Revital H or would it cause any adverse effects in bell's palsy?

MBBS
General Physician, Mumbai
Revital h contains vitamins. Minerals and ginseng. None of them will have any adverse effect on bell' s palsy. In my opinion ion it will be safe to have the medicine.
1 person found this helpful
Submit FeedbackFeedback

I am 88 years for quite a longtime I have numbness on the bottom feet. Taking neurobion regularly no d. M advice.

MBBS, MS - Orthopaedics
Orthopedist, Delhi
Any way rule out diabetes & vit. D deficiency or any other metabolic disorder. Sleep on a hard bed with soft bedding on it. It is because of diabetic/senile neuropathy. Any way take caldikind plus (mankind) 1tab odx10days epineuron sr 150mg 1 tab odx 10 days. Cntact me again for follow up.
Submit FeedbackFeedback

Dementia - 5 Ways Physiotherapy Helps Manage It!

BPTh/BPT, Fellowship in Orthopaedic Rehabilitation (FOR), MBA (Healthcare)
Physiotherapist, Bangalore
Dementia - 5 Ways Physiotherapy Helps Manage It!

Dementia is a general classification of a brain disease that causes a long haul and frequently steady abatement in the capacity to think and recall that is sufficiently incredible to influence a man's everyday  functioning. Other normal manifestations incorporate passionate issues, issues with dialect, and a lessening in motivation. An individual's awareness is not influenced. The most common example of dementia is the Alzheimer's disease.

Physiotherapy for Dementia:
A patient with dementia can benefit from physiotherapy regardless of the possibility that the patient can't perceive their own family. Physiotherapy, notwithstanding, can be of good advantage to the individual who has dementia and also their family and parental figures at different stages. The principle explanation behind this is that recovery administrations can help the dementia patient to be as utilitarian as would be prudent for whatever length of time that is conceivable. Here are 5 ways physiotherapy benefits an Alzheimer's patient:

  1. Physiotherapy can keep up the Alzheimer's patient's freedom and mobility as much as one could expect reasonably. A physiotherapist can outline a home activity program and work intimately with relatives to administer to the Alzheimer's patient.
  2. Physiotherapists, as independent experts, embrace much detailed, separately custom-made appraisals of the disorders, action confinements and restrictions imposed upon individuals with dementia.
  3. The caretakers of individuals with dementia regularly show weakness when contrasted with their same aged companions. Physiotherapy helps with diminishing the weight of consideration by instructing caregivers to provide encouragement and upliftment to individuals with dementia.
  4. Patients with dementia are always at a risk of falling down and hurting themselves. Poor balance accounts for the danger of falls. This can be worked upon and improved by physiotherapy driven exercises. Exercise can have a huge and positive effect on behavioral and mental indications of dementia, enhancing psychological capacity and mindset, which can decrease the doses of strong medicines. Special exercise routines are assigned to the patients which help improve their body balance while walking.    
  5. Physiotherapy has crucial influence in advancing and keeping up portability of individuals with dementia. It assumes a basic part in the end of life consideration by overseeing situations, seating and complicated muscle contracture. Individuals with dementia regularly experience issues in communicating pain. Pain influences cognizance, inspiration and reaction to any intervention. Physiotherapists are specialists in recognizing and treating pain in dementia patients and give training to care home staff and caregivers of the patients.

Physiotherapy is very important for dementia patients. Regular physiotherapy sessions are beneficial for patients for improvement in condition. If you wish to discuss about any specific problem, you can consult a physiotherapist.

4641 people found this helpful

Hi, I am feeling tingling and shivering in my left side arm and leg nearly elbow and knee. I feel this condition from last approximately 10 days. Please let me know what is this?

MBBS
General Physician,
This may be due to the demylination of peripheral nervous system may be duevto some injury you should consult a medical specialist.
1 person found this helpful

My husband is 39 years old male. He had epilepsy problem after head accident (3 times operation of head) from 3 years. Now he take the medicine eptoin 100 3nos. Please advise.

MBBS, cc USG
General Physician, Gurgaon
He need to take this medicine as advised by your Doctor regularly and must not missed dose even for single day Consult Neurologist
Submit FeedbackFeedback

Good day to everyone. I was wondering if I can get some advice before making an appointment to see my doctor. I have quite extensive arthitius in my neck and spine. Painkillers that I am using are working quite well at the God! I have now started to have slight numbness in my.

M.Sc - Psychology, MBA (Healthcare)
General Physician, Kangra
Good day to everyone. I was wondering if I can get some advice before making an appointment to see my doctor. I have ...
most probably you are suffering from cervical spondylitis with radiculopathy... take neurobion forte twice a day.
Submit FeedbackFeedback

Please suggest me what medicines I should take for insomnia. I m suffering from insomnia.

DHMS (Diploma in Homeopathic Medicine and Surgery)
Homeopath, Ludhiana
Homoeopathic medicine PASSIFLORA Q (Dr Reckeweg) Drink 20 drops in 20 ml fresh water in morning and afternoon.Drink 20 drops in 20 ml fresh water before sleep.
Submit FeedbackFeedback

Hello Doctor, My wife who is now 41 years old has a problem with constant headache and mild fever sometimes. I have consulted some doctors but they all give different reasons. Some say its migraine and some say its due to mental tension and a lifestyle which needs to be changed. Please advise.

MBBS
General Physician, Mumbai
Hello Doctor,
My wife who is now 41 years old has a problem with constant headache and mild fever sometimes. I have c...
Few things related to headache so that we can plan the treatment accordingly - if pain is associated with blurred or decreased vision than check your eye sight for refractive error - if the pain is associated with cold and fever than we have to rule out sinusitis as the cause and if the pain is pulsatile in nature and with a throbbing pain usually with an aura than we have to rule out migrane as the cause - if the pain is associated with neck problems than we have to rule out cervical spondylosis as the cause - if the pain is associated with either low or high bp or due to hyperacidity than we have to treat the cause after examination.
Submit FeedbackFeedback

I have JUVENILE MYCLONIC EPILEPSY since 3 years. I came to know about it when I met a neurologist which had me an EEG test. There is no one in my family have this problem. Not even any neurological problem so far. I don't know where I got this disease. Doctor said the cause is unknown. Also I am physically weak. Is weakness might be a cause? I have also other problems such as memory loss, confusion and attention problem. Are these problems due to that disease? I just want to know what's cause of this.

MSC Human Development , Hypnotherapy , Special Educator , ms- counselling and physiotherapy, Applied psychology Hons
Psychologist, Faridabad
Hello sir, there are many causes of epilepsy. It may occur with genes, over stress, brain chemical imbalance, or in a past if you had any head injury for which you are took long term treatment. It is treatable. Thanks.
Submit FeedbackFeedback

1) BACK PAIN:- I'm suffering from back pain since giving birth to my baby boy in 2013. The pain is now increasing day by day. 2) MIGRAINE/SINUSITIS:- I'm also suffering from blocked nose, headache on one side of my head even before my marriage & its still persisting & it'/s also increasing more. Now my age is 26 yrs & i'm housewife.

M.SC. in Sports Injury, BPTh/BPT
Physiotherapist, Mumbai
1) BACK PAIN:- I'm suffering from back pain since giving birth to my baby boy in 2013. The pain is now increasing day...
Hi back pain after delivery of a child is a usual problem for all the mother so hence you have to strengthen your core muscle as due to pregnancy your core muscle are under a lot of stress and goes into weakness. Start taking hot packs twice daily which will reduce your muscle spasms.
2 people found this helpful
Submit FeedbackFeedback

I'm 31 male, have measured 142/92 bp, taking migraine plus and homeopathy too. Now regularly bp coming 120/80 avg. Till how many days I have to take this medicine.

MBBS, MD - Internal Medicine
General Physician, Ghaziabad
Migraine plus tablet is not the drug to lower bp. U have not mentioned homeopathic medicine you are taking fr what reason. U should regularly check your bp for 3 days if consequtivly it is high than you need to be on medication. As your age is not much you require proper evaluation for having high bp. U should consult a physician in person and get investigated properly.
Submit FeedbackFeedback

Hey. I am feeling nervous breakdown every now and then please advise me with proper thing. So I can overcome with it.

MBBS
General Physician,
this is because of your regular stress and strain ,anxiety neurosis . you have to change your lifestyle. and thought process. you have tontake any task atva time you should think about how youvare goingbto accomplish thebtaskthebtask do not think at the same time another task ahead. think it as and when it comes so there is no confusion. have self confidence that cones when you are clear on your goal it will improve.

Numbness in left hand & then left face numbness, ghabrahat hoti hai, dhadakan badhti hai

MPTh/MPT, MSC CVR, MANUAL THERAPIST
Physiotherapist,
Get your cardiac profile checked, may also be a case of cervical spondylitis. Please get assessment done by a cardiologist or a Physiotherapist.
Submit FeedbackFeedback

I am an epilepsy patient. I took medicine daily 3times, but sometime I face the shivering problem. Pls suggest why it's happening and when will I get rid of this problem?

MBBS, MD - General Medicine, DM - Neurology
Neurologist, Hyderabad
Epilepsy is a chronic disease, and it needs medicines for a long time. This would keep seizures under control. Shivering can be a side effect of medication too such as sodium valproate.
Submit FeedbackFeedback

My hand is shaken (more vibrate) during writing. I write right hand. I am 26 year old. Why the reason of vibration my hand. Please suggestion me and how to solve it please help me. I am waiting your answer.

Bachelor of Occupational Therapy (BOT)
Physiotherapist, Mumbai
Hand shaken in many neurological conditions. And sometimes due to weak uncoordinated musclea of hand consult to you r doctor and then to neurologist.
1 person found this helpful
Submit FeedbackFeedback

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
View All Feed