Dr. Amit Kumar Ghosh is a renowned Neurosurgeon in Kolkata. He has been a practicing Neurosurgeon for the past 17 years. He completed his Bachelor of Medicine Bachelor of Surgery (MBBS) from Calcutta National Medical College in 2000. In 2008 he passed DNB-National Board of Examination. He also has a Fellowship in Neurosurgery from Fujita Health University, Japan. Currently, Dr. Ghosh is working as a neurosurgeon at the National Neurosciences Centre, Peerless Hospital and B.K. Roy Research Centre, Kolkata. As a specialist Neurosurgeon he offers the following services: Accident Injuries Treatment, Head & neck Cancer Surgeries, Anterior Segment Surgery, Endoscopic Skull Base Surgery, Brain Suite Treatment, Brain Tumour Surgery, Brain Suite Treatment, Cerebrovascular surgery, Chemonucleolysis treatment, Colitis Treatment, Column Traumatology, CSF Rhinorrhoea Repair treatment, Decompression Microvascular Surgery, Deep brain Stimulation Procedure, Treatment Of Disc Prolapse, Epilepsy Surgery, Epilepsy Treatment, Fracture Treatment and Gamma- Knife Treatment.
Dr. Ghosh is an active member of several professional societies such as the Neurological Society of India, Indian Medical Association (IMA), Asian Congress of Neurological Surgeons, Congress of Neurological Surgeons, Congress of Neurological Surgeons, Congress of Neurological Surgeons and Neurological Surgeons Society of India.
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Treatment of Neurological Problems
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Patient Review Highlights
The speaking disability was quite embarassing for me. I consulted Dr Amit, the speech therapy treatment was very effective. I am quite benefitted with her treatment. Even though the doctor is not from our city, he is still very famous, so we consulted him. He is a well knowledgeable neurosurgeon.
I found the answers provided by the Dr. Amit Kumar Ghosh to be helped me improve my health. thanks a lot for your valuable and excellent guidance
I found the answers provided by the Dr. Amit Kumar Ghosh to be very helpful and knowledgeable. Thanks a lot I thought it is parkinson
Dr. Amit Kumar Ghosh provides answers that are knowledgeable. Thank you doctor
There is hardly any individual who hasn't suffered from back pain at some point or the other, and lower back pain is considered one of the prime factors for which people might want to miss a day of work. The source of the pain could range from herniated disk to muscle spasm to osteoarthritis. What’s worse, it could be benign or cancerous spine tumor. Even though spinal cord tumors are quite rare, when it occurs, it could be life-threatening. If caught early, it is possible to treat spine disorders effectively and therefore, it pays to know a few important facts about spinal cord tumors.
- Back pain is the most common symptom: When it comes to spine tumors, regardless of whether they are cancerous or non-cancerous, you cannot afford to ignore back pain. This is because the tumor causes pain by pressing against the spinal cord or destroying the bone. It is crucial to note that such type of back pain tend to linger even while you are resting at night.
- Pain that radiates to other parts of the body as well: When spine tumors are the culprit for back pain, it can radiate towards the arms or lower back rather than improving with time.
- Spinal cord tumors can lead to other symptoms: There is no reason to believe that when you have spinal cord tumors, then you will only suffer from a debilitating back pain. You may also suffer from reduced sensitivity to pain, difficulty in walking, loss of sensation and muscle weakness. You may also notice that you have a decreased sensation to heat and cold as well.
- People who have previously suffered from cancer are at a high risk: Individuals who had cancer particularly, breast, lung, kidney, prostate, and thyroid should be extra careful about their health in general. You should regularly monitor the symptoms of spine tumors since you are at a higher risk of developing it. It is found that in about 60 to 70 percent of the cases, cancer occurring in other parts of the body either metastasizes or spreads to the spinal cord.
- There are ways other than surgery to remove spinal tumors: A biopsy would be able to tell whether the tumor is malignant or benign. A biopsy is a process which involves removal of a small tissue sample and also examining it with the help of a microscope. But it is important to note here that all spinal tumors do not require an immediate removal through surgery. Sometimes, all you will need is a regular monitoring for detecting if there is any change. This is commonly chosen when the spinal tumors are small and benign.
Not always your back pain is a sign of spinal cord tumor. However, in the case of a persistent back pain along with other symptoms, a doctor’s opinion must be sought.
The sensation of pain and numbness are quite common in patients suffering from high blood sugar. If you are suffering from nerve damage from high blood sugar, chances are you have diabetic peripheral neuropathy. The discomfort can affect your mood and overall quality of life. But with some easy to follow steps can help you keep peripheral neuropathy under control.
- Keep your blood sugar levels under control: Your first task is to manage your blood sugar levels under control and with the passage of time it will damage the peripheral nerves and pave the way for diabetic neuropathy. If you can keep your blood sugar levels within a healthy range, you will be able to reduce the risk of nerve damage by about 60 percent. You should talk to your doctor first since a rapid drop in the blood sugar levels can prove to be even worse.
- Get the right level of Vitamin D: Your skin functions by producing Vitamin D in response to sunlight and it is immensely helpful in shielding against nerve pain. It has been found people who have lower levels of this nutrient are more likely to suffer from more pain. In case it is hard to get the recommended daily intake from food only, you will have to take supplement pills.
- Keep away from smoking: We all know that smoking causes the blood vessels to constrict which hampers circulation. If you don’t quit smoking, your peripheral nerves may not be able to nutrient-rich blood which would make pain worse.
- Take a warm bath: Warm water is not just relaxing, it can also improve circulation all through the body. It can provide instant relief. But it is worthy of mention here that since diabetic neuropathy leads to loss of sensation, you should ensure that the water isn’t too hot before you jump in.
- Seek resort to over the counter medications: There is a host of painkillers available for easing mild to moderate ache stemming from diabetic neuropathy. These include ibuprofen, aspirin, naproxen and acetaminophen. But before taking any of these pills, you should consult with an expert who can choose the right medicine for you.
- Get up and move: Exercise can combat pain in a variety of ways. It helps in keeping blood sugar levels under control which, in turn, can hinder nerve damage. Workout increases blood flow to the extremities while also uplifting your mood. It will help you get rid of stress so that you can better deal with the symptoms of peripheral neuropathy. In a study conducted by the University of Kansas, it was found that people who exercise regularly didn’t face any trouble in doing daily activities.
- Consider carpal tunnel surgery: When the patient is suffering from localized peripheral nerve compression that affects the hands, carpal tunnel surgery can be considered as a last resort to achieve pain relief, reduced incidence of ulceration, increased range of movement and balance, preservation of limbs and improved quality of life.
With these few tips, you will be able to manage the peripheral neuropathy better. In case you have a concern or query you can always consult an expert & get answers to your questions!
Some people suffer from difficulty in remembering things, and this may be attributed to Alzheimer’s disease even though it is not the only cause of memory disorders. If you are recently having troubles in remembering, then it is high time that you should consult with an expert.
Common causes of memory disorders
You will be surprised to know about the various causes of memory loss and here are some of them include:
- Sleep apnea: This is a common yet easily treatable sleep issue which is often linked with dementia and memory loss. You may have sleep apnea if you find yourself waking up with a terrific headache along with fatigue that lingers all through the day. The injury caused by sleep apnea may lead to permanent damage to the brain cells.
- Certain medications: Memory loss may be a sign that the medicines you are taking need to be adjusted. Drugs including sleeping pills, anti-anxiety medicines, painkillers, antihistamines, and diabetes medicine may take a toll on the functionality of your brain. Many studies have suggested that cholesterol and diabetes lowering drugs contain a chemical which gives way to reversible cognitive side effects.
- Silent stroke: When you feel that there is an unexplained inability to think or to move in a normal way, then it could come from a silent stroke. Mild memory issues may also stem from silent strokes affecting smaller blood vessels. These alterations in brain functionality may range from mild to severe and are termed as vascular cognitive impairment.
- Nutritional deficiency: When you substantially lack in Vitamin B12, your normal brain function will be hampered. This may lead to confusion as well as dementia. Every day, you must get 2.4 micrograms of B12 in the diet from fish, meat and dairy products.
Treatment of memory problems
The treatment of memory problems is entirely dependent on the cause. In some instances, the disorder is reversible with the help of proper treatment. For example, when the memory loss is caused by some medicines, it can be cured by altering the course of medications. Treating depression may also be helpful for memory problems when depression is the causing factor.
There are many medicines available for the treatment of memory problems. With the progress of memory problems, the cells of the brain start dying, and it causes the cognitive symptoms to worsen. Even though the medications that are available at present may not be helpful in stopping the damage to the brain cells, they can be helpful in stabilizing the symptoms by influencing the chemicals involved in carrying messages among the nerve cells in the brain. Sometimes, doctors prescribe both the types of medicines together to speed up the recovery process hindering further damage.
In case you have a concern or query you can always consult an expert & get answers to your questions!
The word epilepsy brings to mind visions of people frothing at the mouth and rolling on the ground. However, epilepsy affects each patient in a different way. This can make it hard to recognize at times. In the more serious cases of epilepsy, an epileptic attack can make a patient injure himself or develop other life threatening conditions. In rare cases, epilepsy can even cause death. Thus it becomes imperative to understand how to deal with epilepsy.
Treatment options for epilepsy can be categorized as medication, surgical procedures and dietary changes.
Medication for epilepsy is prescribed on the basis of the symptoms presented and the type of epilepsy the patient is suffering from. In most cases, seizures can be controlled with a single type of medication, but in others, the doctor may need to prescribe a combination of medicines to control epilepsy. These forms of medication do have side effects and hence any reactions to the medication must be immediately brought to the doctor's notice. The dosage for epilepsy medication may need to be varied with time. An epileptic patient should never discontinue medication on their own.
Depending on the type of seizures and the area of the brain affected, a doctor may advise surgery in cases of severe epilepsy. Surgery can help reduce the number of seizures experienced or completely stop them. Surgery to treat epilepsy is of many types. Some of the common procedures are:
1. Surgery to remove tumor of any such conditions that may be triggering the epileptic attacks
2. Surgery to remove a small section of the brain from where a seizure originates. This may also be referred to as a lobectomy.
3. Multiple subpial transaction or a surgery that involves making a series of cuts in the brain to prevent the seizures from spreading to other parts of the brain.
4. Surgery to sever the neural connections between the right and left hemispheres of the brain.
5. Surgery to remove half the brain's cortex or outer layer
A diet rich in fats and low in carbohydrates can help reduce seizures. This is known as a ketogenic diet and aims at making the body break down fats instead of carbohydrates. It can cause a buildup of uric acid in the body and thus should be practiced only under the guidance of a dietician. In cases where epileptic attacks are triggered by malnutrition and birth defects, taking vitamin supplements can help lower the frequency of seizures.
In case you have a concern or query you can always consult an expert & get answers to your questions!
Undergoing Brain Surgery can be a very traumatic experience, and it is common for many patients recovering from brain surgery to face depression, spells of dizziness, confusion and weakness post the surgery. It can be very critical that family members and friends talk to the patient and be empathetic towards them.
It takes approximately 12-18 months for the brain to heal after a brain surgery and slowly and gradually the patient will regain all his normal functions and get back to his daily routine. However in that time they need the complete support and understanding of their families, as well may need help from therapists. This will help the patient in gaining back their independence as well as confidence in their abilities.
Here are some tips that will help you deal with a patient recovering from Brain Surgery:
After brain surgery, a person may feel disoriented and have some speech or understanding disability for a while. Family members and friends are advised to take pause when talking to the patient, so that he/she can easily understand the conversation. Speaking slowly is not recommended, as patients may recognize it and have an emotional outburst or feel hurt.
Caretakers and family members should also keep reminding the conversation topic at different points to the patient, so that it is easier for them to participate in the conversation.
Family members should also not react adversely in case of emotional outbursts, instead show love and patience to a person recovering from brain surgery.
Caregivers should make sure that the person recovering from brain surgery gets enough sleep and rest to recuperate.
People interacting with someone recovering from brain surgery should understand that the person's ability to learn and remember will improve daily, and any lapses in attention by the patient are not caused by any act of obstinacy. Your care and understanding will be essential for a person to recover.
Family members should also make sure just to give enough care and not smother the brain surgery survivor. It is essential for them to regain their confidence and a sense of competence.
Family members should take the patient for a neuropsychological examination--after treatment, 6 months later, and a year later to see if they are recovering properly. Caregivers should watch out for emotional outbursts, like rage, uncontrollable laughter, withdrawal and depression. In case of such symptoms it is advisable to take the patient for a check up with medical practitioner. If you wish to discuss about any specific problem, you can consult a Neurosurgeon.
Sciatica refers to the pain one experiences due to the irritation or compression of nerve roots contributing to formation of Sciatic nerve. The sciatic nerve is the longest and widest nerve in the body, running from the lower back, down to the back of each leg. The pain can occur in the lower back and spread to the hips, buttocks and leg. Sciatica generally affects one side of the body. There are numerous causes of irritation of the sciatic nerve and sciatica.
Some of them are:
- Spinal Stenosis: The narrowing of the spinal canal caused by natural wear and tear of the vertebrae (individual bones in the spine protecting underlying nerves) of the spine is known as spinal stenosis. The narrowing may put pressure on the roots of the sciatic nerve, causing pain.
- Herniated Disc: A disc is made up of cartilage and acts as a cushion between vertebrae, allowing flexibility of the spine. A herniated or slipped disc occurs when a disc is temporarily pushed out of place, putting pressure on the sciatic nerve.
- Spondylolisthesis: It is a condition where one of the lower vertebrae slips forward over another. This also causes a collapse of the disc space between both, causing the nerve to get pinched. This may cause sciatica.
- Piriformis Syndrome: Piriformis is a muscle found deep inside the buttocks, which connects the lower spine to the upper thighbone, running directly over the sciatic nerve. Spasming of this muscle can pressurize the sciatic nerve, triggering symptoms of sciatica.
- Sacroilitis: Sacroillac joints are the place where the lower spine meets the pelvis and inflammation of one or both of these joints causes sacroilitis. This can give rise to symptoms of sciatica as it causes pain in the lower back, buttocks and legs.
- Spinal tumors: Very rarely, tumors growing inside or along the spine may put pressure on the sciatic nerve.
- Infection or injury: Muscle inflammation, infections, fractures or any other spinal injury may lead to irritation or compression of the sciatic nerve.
- Pregnancy: Pregnant women may suffer from sciatica due to weight gain, expansion of the uterus or increased fluid retention or other changes occurring in the body, which put pressure on the sciatic nerve.
- Other causes: Osteoarthritis and fractures caused by osteoporosis may also affect the sciatic nerve, producing symptoms of sciatica. If you wish to discuss about any specific problem, you can consult a Neurosurgeon.
Epilepsy is an abnormal medical condition due to abnormal electrical discharge from the brain, which could be due to genetic defects, brain injury,brain infection,brain tumor etc.
Recent study shows, patients with awareness, knowledge and attitude towards the disease had better health related quality of life.
- Do take your medicines at the prescribed times.
- Do make it known to your family members, friends and people who work with you that you are seizure-prone. Tell them what should be done in case you get an attack in their presence. This is nothing to be ashamed of as epilepsy is a medical condition just like high blood pressure. If your child has epilepsy, do inform the teacher and the school authorities about it.
- Do tell your child's teacher what to do if your child has a seizure.
- Do keep an accurate record of your seizures and their frequency. Preferably, maintain a seizure diary.
- Do ask your doctor about medicines for other conditions before taking them.
- Do follow a balanced diet.
- Do exercise regularly but avoid over-exertion.
- Do have good lighting in the room where you watch TV. TV picture flashes can trigger seizures. Good lighting can prevent such attacks.
- Do tell someone if you are going for a swim; swim only if your seizures are under control. Moreover, whenever possible, go swimming with a friend.
- Do talk to your doctor about the pros and cons of using contraceptive pills (medicines used by women to avoid unwanted pregnancy) along with your epilepsy medicines.
- Do wear protective headgear when cycling.
- Do tell your doctor about any ill effects that you experience.
- Do get a good night's sleep daily.
- Do make sure you have enough medicine so that you don't run short, even when you are travelling.
- Do check-in with your doctor regularly.
- Don't stop your treatment unless your doctor tells you to.
- Don't consume caffeine or alcohol excessively.
- Don't take other medicines without checking with your doctor.
- Don't lock the bathroom/toilet door, if possible.
- Don't smoke.
- Don't give others your medicines and don't take anyone else's medicines.
Myths and facts about epilepsy
Is epilepsy a very rare disorder?
No. Epilepsy is not a very rare disorder. Epilepsy affects 50 million people worldwide. In India, epilepsy has been identified as a public health problem.
Epilepsy is a mental illness?
It is not a mental illness but disorder of the brain.
Are people with epilepsy violent or crazy?
No. The belief that people with epilepsy are violent is an unfortunate image that is both wrong and destructive. People with epilepsy have no greater tendency toward severe irritability and aggressive behaviours than other people. However, once the attack is over, they return to normalcy and usually display normal behaviour in between attacks.
Are children with epilepsy dull?
Except for children who are born with obvious mental handicaps, children with epilepsy have normal intelligence and should be encouraged by parents and teachers to attend school and complete their education.
Is epilepsy a curse or wrath of God?
No. Epilepsy has nothing to do with curses, possession or other supernatural processes, such as punishment for past sins.
Does epilepsy spread through touching or coughing?
No, epilepsy does not spread through touching or coughing.
Does the use of an onion, metal, etc., help in terminating an ongoing epileptic attack?
No. Some people think that an epileptic attack can be terminated by making the person smell onions or dirty shoes, or by placing a metal key in the person's hand. These are irrational beliefs.
Are epilepsy medications ineffective?
No. Epilepsy medicines are very essential for the control of epileptic attacks and should not be neglected.
Is marriage a cure for epilepsy?
No. Marriage is an important aspect of life but not a cure for epilepsy.
Epilepsy is hereditary hence unfit to get married?
Epilepsy is not a hereditary disorder, and the tendency of epilepsy being passed is only about 3 %, therefore no bar for marriage.
Women suffering from epilepsy cannot have children?
Epilepsy or anti-epileptic drugs cannot affect fertility, even during pregnancy, women can take their medicines under their doctor’s supervision.
Is life of a person with epilepsy miserable?
No. Life of a person with epilepsy can be very manageable and very similar to life of people without epilepsy provided you have a positive approach towards life.
Is epilepsy a hindrance in leading a happy and successful life?
No. People with epilepsy can live a happy and successful life. With the advent of newer medicines, availability of medical care and increased awareness of the condition, it has become possible for a person with epilepsy to lead a good life. There are many famous poets, writers and sportsmen with epilepsy who have excelled in their respective fields.
Special Precautions in Children with Epilepsy
Computerized and Lights:
Up to 5% of children with epilepsy have photosensitive epilepsy. Computers and TVs with a flat screen do not flicker and, so, are less likely to trigger seizures than screens that flicker. However, flashing lights/ flickering screen can act as trigger in photosensitive epilepsy patients.
Exams and Tests:
For Children who are likely to have seizures in stressful situations or at certain times of the day, this may affect how they perform in exams or tests. Tiredness, memory or concentration problems may also affect exams or tests. Tiredness, memory or concentration problems may also affect exams.
Physical Activities and Lessons:
Safety is important for all children, especially during physical activities and lessons, such as when studying science. Epilepsy does not need to stop a child from doing an activity as long as he or she is safe.
This must be allowed only in the presence of trusted lifeguards. It is essential that the swimming coach and the lifeguards fully understand a child’s epilepsy so they can quickly see if the child is having a seizure in the water.
Please help me out. I had seizure 3.8 years ago and after it my treatment get started as CTSCAN was normal but there were focal bilateral temporal spikes noticed in EEG. I have completed the treatment of three years without any further seizure and till 3 years I was on same dosage of medication, on completion of treatment EEG was again performed and as per doctor there was bit improvement but still like Right focal temporal spikes noticed, Since I was seizure free so doctor asked to stop medication by decreasing the dosage gradually. In mid March I have stopped medication and I am seizure free till date. Since there is no guarantee in medical science but still I have few questions coz I am bit depressed and worried. 1.This seizure indicates I am suffering from epilepsy or it is possible that a person had one seizure only in life time and get cured after treatment? 2. precautions I have to take so seizure will not trigger again or any home remedies/supplements which I take to cure this?
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
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 ---
No of patients
Deuschl et al., 2006
QOL better with DBS, motor symptom better with DBS
Weaver et al., 2009
BL STN or GPi
Dyskinesia free ON time better with DBS
Williams et al., 2010
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.
Idiopathic PD ( No PSP/MSA/NSD etc)
Poor/adverse response to drug
Degree of disability(UPDRS part III score)>25
LEVODOPA CHALLENGE RESPONSE POSITIVE
(30% improvement in UPDRS after 12-hours off medication)
long term anticoagulation
Willing for surgery and programming
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.
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.
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).
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).
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.
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.
Parkinson's disease is a neurodegenerative condition that affects your brain cells which produce dopamine and thus hampering all kinds of motor functioning and other emotional responses. After the disease is diagnosed, medication and therapy can help to provide relief from the symptoms to a large extent but a permanent cure is not possible.
The disorder does not have a definite set of causes. A small percentage of the cases have been related to hereditary factors and others have a range of environmental causes associated with them.
1. Genetic factors:
Specific gene mutations and gene variations have been proved to cause Parkinson's, such as SNCA, PARK2, PARK7, PINK1 and LRRK2. These make or recycle proteins which are linked to the disease.
Research shows that men are at a 1.75 times greater risk of developing the condition than women are. Also, age plays a role with most cases occurring after the age of 60.
2. Environmental factors:
Regular exposure to inorganic insecticides, pesticides, herbicides and heavy metals or other toxins may cause the disorder. In rare cases, Parkinson's disease occurs in the aftermath of a severe head injury or immune disorders.
The symptoms can be classified into two broad categories-
1. Motor symptoms:
- The hand tremors when in resting position
- The grip loosens
- Walking slows down
- Facial muscles freeze partially
- Speech is slurred
- Balance is disturbed
- Swallowing is painful
- Urination is abnormally frequent
- Dementia-like symptoms are seen
- There is involuntary twitching of the fingers and toes
- Repetition of the same movement in quick succession is nearly impossible
2. Non-motor symptoms:
- Dental problems
- Vision impairment
- Skin disorders
- Panic attacks
- Excessive secretion of saliva
- Extreme weight loss or gain
- Sexual problems
- Loss of sense of smell
- Lowering of the pitch of the voice
If you wish to discuss about any specific problem, you can consult a Neurosurgeon.