Parkinson’s disease: Management-a quick one on one

In this blog post let us dwell on the management of Parkinson’s disease (PD). As stated earlier PD is a progressive neurodegenerative disease. This means that as of now PD CANNOT be cured. Once the disease begins it slowly but surely progresses. The rate of progression varies from patient to patient. While PD cannot be cured, there are a number of medications available which can control the symptoms of PD. At times the response with these medications is dramatic and very gratifying. A few salient points:

NOT every patient of PD needs to be treated. When PD initially begins the symptoms are usually mild and may cause minimal interference to the patient’s lifestyle. The mild tremor of PD might be dismissed by the patient as a mere nuisance. At this stage of the disease, the patient does not exhibit problems with his/her gait or balance. The rigidity, bradykinesia is not disabling. At this stage of the disease, the neurologist may opt to simply keep the patient under observation. The patient and the family are educated about the disease and instructed to remain in follow up (come for follow up appointments after very 3-4 months).

The most effective medication for the treatment of PD is LEVODOPA. Since PD is caused by deficiency of dopamine in the brain, the most effective way to treat it is to give dopamine from outside. So levodopa is administered in tablet form usually 3 times a day. Levodopa is combined with another chemical called carbidopa which helps to prevent the breakdown of levodopa in the stomach and thus ensures that high level of levodopa is absorbed and reaches the brain. This combination of LEVODOPA+CARBIDOPA is the main medication used to treat PD. LEVODOPA+CARBIDOPA combination tab is marketed by many different pharmaceutical companies under different names (Please check the common brand name of this combination in your country). The tablet is usually started at low dose three times a day. The neurologist then titrates the dose up based on clinical response and side-effects. The medication is usually well tolerated by most patients and the effect is gratifying. It is important to emphasize that this medication still remains the MOST effective medication for PD. LEVODOPA comes in many different formulations including now in an inhaled form. These formulations are prescribed as the disease advances. Please discuss the same with your neurologist.

DOPAMINE AGONISTS: is another class of medication commonly used to treat PD. As the name suggests medications in this class act by stimulating dopamine receptors in the brain. While not as effective as LEVODOPA+CARBIDOPA, dopamine agonists are commonly prescribed. Commonly used dopamine agonists include pramipexole (Mirapex), rotigotine (Neupro), and ropinirole (Requip). Some neurologists prefer to use a medication in this class as first line treatment and use LEVODOPA+CARBIDOPA when PD symptoms are more bothersome (PD is more advanced).

Amantadine is another medication used to treat PD. It is usually used in combination with either LEVODOPA+CARBIDOPA or DOPAMINE AGONISTS.

Anticholinergic drugs such as benztropine and trihexyphenidyl are also commonly used. These drugs are helpful in controlling symptoms such as tremor and muscle stiffness.

Drugs referred to as selective MAO B inhibitors such as selegiline are used by neurologists usually early in the disease course. There is limited evidence to suggest that medications in this class may be “neuroprotective”.

COMT inhibitors: another class of medications used in the treatment of PD.

Neurostimulator such as DEEP BRAIN STIMULATOR (DBS): A neurostimulator called DBS is sometimes implanted in PD patients. DBS is usually implanted in the brain of PD patients with advanced disease who are experiencing motor fluctuations, medication side-effects called dyskinesias and medication refractory tremor. Please discuss this further with your neurologist.

While medications form the cornerstone of treatment of PD, there are a number of other simple interventions which are very effective. It is important to remember that PD affects the motor system causing problems with gait and balance. Hence I make it a point to emphasize the importance of exercise to my patients and their family. Exercises which improve gait and balance are the most helpful.

dance is a good exercise for patients with PD. (USEFUL RESOURCE:

–many are surprised to find out that boxing is a good exercise for patients with PD (USEFUL RESOURCES: and

–yoga is also a good form of exercise-it improves balance and helps reduce the stiffness in PD patients)

Parkinson’s disease patients are prone to falling. Hence falls are an important cause of morbidity in patients with PD. So simple interventions designed to reduce the risk of falling are helpful. (USEFUL RESOURCE: NATIONAL INSTITUTE ON AGING: Fall proofing your home,your%20way%20when%20you%20walk.)

Nitin K Sethi, MD, MBBS, FAAN

Director and Chief Coordinator Brain Care Foundation (

Please support ongoing research in PD and more importantly PD patients and their families. Source of image is

I have infrequent seizures: to treat or not to treat? -that is the question

A great question from a concerned sister. My reply follows.


Hi Dr Sethi,

Thank you for your very informative site. My brother was recently diagnised with complex partial epilepsy. His seizures (that he is aware of at least) are very few and far between, on average one every two to six months. He says he knows in advance when the sezures are beginning as he starts with loss of vision slowly in one eye and then the other and then his hands go numb.

He feels that the side effects of the medication interfere with his busy schedule and active lifestyle and has opted not to take any medication due to the long periods between seizures. Is this advisable? If his condition is left untreated could it progress or cause any irreversible problems?

Thank you,



Dear K,
you have asked a very valid question and one that I have confronted personally at many times as a neurologist and epileptologist. If seizures are few and far inbetween do they warrant to be treated? There is no consensus on this. Let me explain in my usual simple way.

Argument in favor of not treating them:

1. At times patient’s get an aura and know their seizure is coming and feel they can take precautions such as sitting down if they are standing or pull over to the side of the road if they happen to be behind the wheel of a car when the aura starts. So the patient feels that since he has only infrequent seizures and that too accompanied by a reliable aura, why take an anticonvulsant medication.

2. Moreover every anticonvulsant has its own side-effect profile. Frequently the side-effects are unpleasant and so if possible the patient would like to avoid taking the medication on a regular basis.

3. Anticonvulsants have to be taken on a daily basis, some medicines have a twice daily or three times a day dosing. This interferes with their lifestyle.

4. If the seizures are few and far inbetween (like for example a patient who suffers one seizure every year), does it make sense to take a medicine on a daily basis (at times with unpleasant side-effects)?



Arguments in favor of treating these infrequent seizures:

1. One of the biggest problems with seizures is their unpredictable nature. A seizure can occur anytime, sometimes out of the blue when the patient least expects it. Moreover one does not want to have a seizure at the wrong place and the wrong time like for example when one is driving or when one is waiting by the side of the rail track or when one is swimming. Seizures can be associated with falls and injuries. Hence it makes sense to treat the seizures and aim for good seizure control no matter how infrequent the seizures may be. Many patients feel more confident when they know they are on an effective anticonvulsant and shall not have a seizure out of the blue.

2. In majority of the countries there are laws with respect to driving if you suffer from epilepsy. A patient may not like to risk loss of his driving privileges and independence if a seizure was to occur. He would rather take an anticonvulsant on a daily basis no matter how infrequent his seizures.

So you can see there are good arguments on both sides. Your brother’s doctor shall be the best person to turn to for advice.

Personal Regards,

Nitin K Sethi, MD

I have multiple sclerosis. Do I need to take MS medications? Discussing the pros and cons

Nitin K Sethi, MD


Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065



The decision of taking MS medications is one which requires consideration of multiple factors by both the patient as well as the treating physician. At times the decision to go on medications is relatively straight forward, at other times it requires consideration of multiple factors before deciding on the best course of action.

Let me try to explain this by using a 29-year-old patient whom we shall refer to as Janet.


Seizures due to hypoglycemia (low blood sugar)

Seizures in the setting of hypoglycemia are well described. The brain needs sugar to function and when the blood sugar falls “too low”, one of the things that can happen is that the patient may have a seizure (this is usually a generalized convulsion-a tonic-clonic or Grand Mal seizure). There is no one level of blood sugar below which one has a seizure (rather the level varies from person to person). Let me explain that with an example. Lets assume you are a diabetic and you take your insulin shot but for once forget to take a meal (maybe you are a hard working executive on the run). You have a convulsion while at work and are taken to the nearest ER. There your blood sugar at the time of presentation is recorded to be 60 mg/dl. There might be another similar patient whose blood sugar falls to 52mg/dl yet he does not have a convulsion. So there is no set limit below which the brain shall have a seizure but speaking in broader terms usually the brain does not tolerate blood sugar below 60mg/dl and below 40 mg/dl most patients shall be symptomatic (either have a convulsion or be confused and obtunded. The term used for this constellation of neurological signs and symptoms as a result of hypoglycemia is NEUROHYPOGLYCEMIA).

The good news though is that seizures due to hypoglycemia are readily treatable. In the ER we load the patient with glucose (usually this is given via an intravenous drip as the patient is obtunded and confused and cannot accept anything from the mouth). The blood sugar quickly rises and the seizures stop. Patients who suffer from hypoglycemic seizures do not need to be on an anti-epileptic drug. These patients do not have epilepsy. If their blood sugar does not fall down again, they will not have another seizure.

Rather a meticulous search should be conducted to find out the cause of hypoglycemia:

-is the patient a diabetic who took too much insulin by mistake?

 -did he miss his meal but took his insulin?

-is there any other cause of hypoglycemia such an insulin secreting tumor?

-is the patient septic?

Hypoglycemic seizures are most commonly seen in diabetics. This emphasizes the importance of good glycemic control in this vulnerable population.

Nitin Sethi, MD

Seizures associated with alcohol intake

In this post I thought I shall discuss the effects of alcohol on the brain especially with respect to seizures. Many people drink socially , a drink or two after work is not only relaxing but also enjoyable. But who is an alcoholic or rather when does one have a drinking problem? We doctors use the CAGE criteria as a rather simple questionaire to determine if someone has a drinking problem.

“CAGE” where each letter has a question attached to it and the person has to answer yes or no. Let me elaborate a little.

C–stands for “cutting down”–have you ever felt the need to cut down on your drinking?

A–stands for “anger”—have you ever felt angry if someone has questioned your drinking habit?

G–stands for “guilt”—have you ever felt guilty about your drinking?

E– stands for “eyeopener”–have you ever taken a drink first thing in the morning?

If the person answers yes to these questions, he or she may have a drinking problem. What though is the effect of heavy alcohol drinking on the brain? Does it actually kill brain cells (neurons)? Does it lead to dementia? Can too many drinks cause a seizure?

Alcohol contrary to popular beliefs is a CNS depressant and not a stimulant. Alcohol is rather rapidly absorbed through the lining of the stomach and enters the blood stream from where it is carried to the brain. In the brain, it acts on the neurons and initially causes a loss of inhibition. You loosen up, your speech flows more smoothly and soon you become the life of the party. Well as you continue to drink, alcohol then starts depressing the central nervous system (CNS) . People usually fall asleep soon after consuming alcohol.

But let us get back to how chronic alcohol intake affects the CNS especially with respect to seizures.

I shall discuss this one by one.

Alcohol induced seizures


 Heavy alcohol consumption can induce seizures. Alcohol induced seizures are of different types. One is what is commonly referred to as “rum fits”. Let me explain with an example. You are out with your friends celebrating a promotion. Your drink for the night is beer. Your normal “limit” is say 4 beers. But hey you are celebrating and so you end up binging. Before you know it you are on your 10th beer of the night. Right as you are having your 11th beer, your eyes roll up and you have a big generalized tonic-clonic convulsion (see my posts on epilepsy on my website . This kind of seizure which occurs at the height of binging is what has been referred to as a “rum” fit. I guess it was first described with respect to rum. Any of us can have a rum fit if we drink too much alcohol. You do not need to be an epileptic to have a rum fit, though I feel these kinds of seizures associated with alcohol binging are more common in patients who have an underlying seizure tendency. Thus if you are an epileptic you are more likely to have a rum fit if you overindulge in alcohol as regards to someone who does not have a seizure tendency. Hence I always advise my seizure patients to drink alcohol in moderation. You can drink and by all means enjoy your occasional drink but do not overindulge in this pleasure. Know when to say no and walk out of the bar.

Another type of seizure associated with alcohol is what is called “Alcohol Withdrawal Seizure”. Here the seizure occurs in a different scenario. Usually the person is one who is a chronic alcohol drinker, one who is dependent on alcohol and feels uneasy and restless if he does not drink everyday. Let us now assume he suddenly stops drinking for whatever reason. Maybe he runs out of money and cannot buy alcohol. Usually 24 to 48 hours after his last drink, this patient may have a generalized tonic clonic convulsion. As this seizure occurs in the setting of a withdrawal from alcohol, it is called alcohol withdrawal seizure. It is important that heavy and chronic alcohol drinkers keep this is mind and do not suddenly stop drinking. If a person does decide to quit alcohol he should do it under medical supervision.

Now for the third setting in which seizures might occur with alcohol. Again we have a person who is an alcoholic (heavy and chronic alcohol user). Again for some reason he suddenly stops drinking. Uusally after 72 hours, he starts becoming delirious (confused), he has autonomic dysfunction and is tachycardic, sweating profusely, his blood pressure is up. Such a patient is said to be in what we refer to as “delirium tremens” (DT) . Patient who are in DT may have a flurry of seizures one after the other. DT is a life threatening condition and a patient may die if not treated in time. Usually patients are admitted to the intensive care unit of the hospital. We hydrate them aggressively, we give them medications to calm them down. Lorazepam (Ativan) or other benzodiazepines like chordiazepoxide (Librium) are given to prevent seizures and treat acute alcohol withdrawal.

Patients who have had a rum fit, an alcohol withdrawal seizure or even DT do not warrant long term treatment with an antiepileptic drug. These patients do not have epilepsy. If they abstain from drinking in the future it is more than likely that they may never have a seizure again in their lifetime. However there are a few patients whom we feel have a high risk for seizure recurrence, in such patients we may prescribe antiepileptic drug therapy for some time (the duration of the therapy varies depending upon the history, examination findings and the results of investigations like EEG and CT scan or MRI brain)

I have tried to give an overview of the kinds of seizures associated with alcohol intake. Like I stated earlier one need not be an epileptic to have seizures associated with alcohol intake. I try to explain this to my patients as follows. The brain has a threshold for the amount of alcohol it can tolerate. This threshold varies from person to person. If you drink above that threshold, the brain does not like it and one way it reacts is by having a seizure. This “threshold” is lower in patients who have an underlying seizure tendency. In these epileptic patients, a small amount of alcohol may induce a seizure. Also if you mix your drinks or combine alcohol consumption with other recreational drugs like cocaine you are creating the ideal grounds to have a seizure. Certain medicines like antibiotics also lower your seizure threshold and hence should not be used along with alcohol.

Patients with epilepsy should discuss about alcohol consumption with their doctors because at times we doctors do not initiate this discussion of our own. If you have seizures my advise to you would be to drink in moderation and not exceed your limits.

Nitin Sethi, MD

Carpel Tunnel Syndrome (CTS)

Let us talk here about carpel tunnel syndrome (CTS), a relatively common neurological condition involving a peripheral nerve namely the median nerve. The median nerve is a long nerve which originates from the brachial plexus and runs down the arm and forearm. As it cross from the forearm to the wrist, it goes into a tunnel formed by the transverse carpel ligaments. This tunnel is called the carpel tunnel.

CTS refers to the condition when the median nerve is pinched as it tranverses the carpel tunnel. Hence CTS is nothing other than a compressive neuropathy of the median nerve across the wrist (the site of compression of course is the carpel tunnel). So what do I mean when I say compressive neuropathy? Simple it means due to external pressure on the nerve, the nerve gets compressed. When the nerve is compressed there is interruption in the flow of signals across the nerve. This causes a neuropathy and presents clinically with neuropathic symptoms. So how does CTS present clinically?

–patients may have complain of numbness involving the area of the thumb and the first two fingers (index and middle).

–at times they may not complain of numbness per se, rather have burning, tingling, pins and needle sensation and at times frank pain in the same distribution. This is especially prominent at night and may keep them from falling asleep..

–if CTS is severe, patients may develop weakness and have difficulty in gripping things or making a fist. Severe CTS causes atrophy (weakness) of the mucles supplied by the median nerve.

Etiology of CTS:

So lets now discuss some of the causes of CTS. CTS occurs when the carpel tunnel gets narrowed and the median nerve starts getting pinched. There are many causes of CTS. One of the most common is job or occupation related. CTS is frequently seen in people whose job involves repetitive motion of the wrist-just as excessive typing (manual and/or the computer), washing clothes with your hands (wringing motion of the wrists as you try to squeeze the water out) are a few of the examples.  Other causes of CTS include:

1) Rheumatoid arthritis (especially if the arthritis involves the wrist).

2) Pregnancy: CTS is more common during pregnancy. The thinking is that during pregnancy, weight gain occurs and this somehow narrows the carpel tunnel.

3)Amyloidosis: patients who have amyloidosis are more prone to getting CTS.

4) Acromegaly: patients who have acromegaly ( due to excessive secretion of growth hormone from the pituitary gland) again are more prone to CTS.

5) CTS may occur after trauma or fractures involving the wrist joint.

Diagnosis and management of CTS:

The diagnosis of CTS is clinical. Your doctor shall be able to diagnose if you have CTS on the basis or your history and clinical examination. Usually no other testing is warranted. Unless there is a doubt in my mind, I do not order tests like nerve conduction studies or EMG (electromyogram or needle study). Nor is there a need to have a MRI scan of your neck. Your doctor may order one if there is doubt that the nerve is not pinched at the wrist rather higher up in the neck (this though should be detectable from the history and clinical examination).

Once the diagnosis of CTS is made, the treatment depends upon the cause. The patient is advised to avoid activities like typing (this may be difficult to avoid all together especially if it a part of your job). In any case either by modifying the way you position your hands or the amount of time you spend on the computer some benefit can be obtained. Initial treatment of CTS is usually conservative. Your doctor might advise some conventional pain medications like ibuprofen. Using wrist spints also helps and I advise my patients to wear them at night too while asleep. Patients are usually referred for physicial therapy so that they can learn better hand ergonomics. The role of injecting steroids into the carpel tunnel to lessen the inflammation is unclear. They likely do provide some relief though for a short time. Most patients recover with the above. In a few severe cases especially the ones which have weakness, surgery may be needed. The surgery usually involves cutting the carpel ligaments and making space so that the pressure on the median nerve is removed and that it can breathe.

I hope this helps some of you.

Personal Regards,

Nitin Sethi, MD

Parkinson’s disease: when to treat and how?

Recently I was asked by someone when should we treat a patient with Parkinson’s disease, early on in the disease course or later when the clinical symptoms are more florid? As you know Parkinson’s disease is a progressive neurodegenerative condition characterized by tremor (resting tremor of the limbs, see my post on tremors, rigidity (stiffness), bradykinesia (patients have less spontaneous movements) and a characteristic disturbance of gait and posture (patients walk stooped forward and their balance is off, making them more prone to falls).

As you can well imagine all these symptoms do not start off all at once. Infact the onset of Parkinson’s disease is quite insidious and generally asymmetrical. In its earliest stages, all the patient may have is a unilateral (one hand) tremor. Later as time goes by and the disease progresses the symptoms become more florid and the bardykinesia and disturbance of gait and posture appear.

So that brings us to the question of my post, just when do we start treating these patients? Should we treat them early or should we treat them in the later stages?

There is no good answer to this question. One concern which has been raised is that if you treat patients with Parkinson’s disease with levodopa/ syndopa (the combination is called Sinemet in The United States), early on in the disease course, the drug itself may hasten the progression of the disease (the thinking behind this is the concern that levodopa may increase the breakdown of dopamine secreting cells in the basal ganglia).

On the other hand, there is some evidence to suggest that early treatment is better because it prevents the compensatory change in hardwiring which occur in the brain in the face of decreasing dopamine (some of the neurons such as that of the subthalamic nucleus become overactive in the face of decreasing dopamine secretion and this later on leads to more problems such as the on-off phenomena).

So what is the answer? I think a patient should be treated when he devlops symptoms that start bothering him or interfere with his functioning and activities of daily living. If that occurs early in the disease course, so be it, he warrants treatment. Nowdays apart from levodopa/syndopa (Sinemet) there are many other drugs which can be used to treat the disease especially in the early phases. These drugs ( dopamine agonists like Requip (Ropinirole) and Mirapex (Pramipexole) and selegine) are less stronger than levodopa/syndopa combination but are thought to have less “neurotoxicity” and hence are preferred to be used in the early stages of the disease.

Your doctor shall help you navigate these questions. Have a good weekend everyone. It is Saturday morning here in NYC as I pen this, I think I shall go for a run.

Personal Regards,

Nitin Sethi, MD

Brain tumors: malignant gliomas

Thank you for sharing your brother’s history with me Franciso, I understand how difficult it must be for you and the entire family. I wish him my very best and please feel free to contact me here if you have any particular questions related to him.

Let me continue a little about the management of brain tumors. Well like I said once we discover a glioma in the brain, we first try to determine its extent in the brain. Tests like CT scan and MRI brain  with contrast (dye) are carried out to determine its boundries. Then the question of staging the tumor arises. At times from the MRI itself one can be reasonably sure that this is a malignant glioma or GBM. GBM is one of the few brain tumors, that can spread to the underside of the brain via the corpus callosum and hence gives rise to what we call a butterfly lesion on the MRI (imagine a butterfly with her wings spread out). GBM usually have a lot of surrounding edema which we can see on the MRI again hinting that is a malignant tumor we are dealing with.

Low grade tumors usually are walled off (encapsulated) and do not much surrounding edema. So the next step is trying to stage the tumor and trying to determine its grade. For this reason at times a brain biopsy is done. At the time of the brain biopsy, a frozen specimen is sent to the lab and if the lab gives its initial impression as a tumor, the surgeon might try to debulk the tumor right then and there (that means at the time of biopsy, try to debulk the tumor. This makes sense because the skull is already open and it avoids a second operation).

There is one issue here which is unique for brain tumors like gliomas. The tumor may have one grade on one side and another grade in a different part of the tumor (meaning one part of the tumor may show grade II and the other grade III. To overcome this problem multiple biopsies are taken from different parts of the tumor. The highest grade found is the final grade given to the tumor).

Like I said earlier depending upon the stage of the tumor and its location, the surgeon may or may not be able to remove the entire tumor.

After the biopsy/ surgery patients undergo rehablitation and are then referred to either radiation oncology for radiation or to an oncologist for consideration of chemotherapy. Most of the times all these facilities are available under one roof in a big hospital.

I shall touch on the finer aspects of radiation and chemotherapy in my next post. Its 7.00 pm sat evening NYC, do not have any major plans but do want to get to the gym at some point. Hope all is well in the big world around me.

Personal Regards,


Brain tumors: malignant glioma

Since the diagnosis of Ted Kennedy with a malignant glioma, the focus has again turned to brain tumors. Let me discuss in this post a little about malignant gliomas. Glioma are one of the most common primary brain tumors. They are called gliomas because the tumor arises from the glial cells (the tumor does not arise from neuronal cells, rather from glial cells which form the structural supporting cells in the brain).

The WHO (world health organization) grades gliomas into 4 classes:

1) Grade I and II gliomas: are also what are called low grade gliomas. These are slow growing tumors, usually seen in the younger age groups. As they are slow growing, they are less malignant and compatible with a longer survival. They ususally present clinically with a seizure (when they irritate the underlying brain) or when they grow in size and become large, they present with mass effect (the mass and bulk of the tumor presses on surrounding structures and patients may present with weakness on one side). How are low grade gliomas treated?

Treatment of low grade gliomas; as these tumors are slow growing, they are at times amenable to surgical resection. This is because these tumors are usually well encapsulated and its margins are well defined. So in children or adults, if we catch these tumors in time and if the tumor does not involve the eloquent cortex (parts of the brain which subserve speech, or control the hand and leg movements), one may be able to resect the entire tumor out enbloc. In some patients, that is all what may be needed and we usually like to avoid radiation in children ( since radiation has its own problems and may cause cognitive deficits in the young child later on). You doctor may also put you on an anti-seizure medication for a short while to prevent you from having seizures.

Grade III and IV gliomas: or high grade gliomas. This includes glioblastoma multiforme or GBM. Since these tumors are high grade, they are usually fast growing and invade the surrounding brain tissue. Hence it is impossible to resect the entire tumor out usually. Even if you resect the entire tumor you see macroscopically (that is with the naked eyes), the tumor has already caused microscopic metastasis and spread in the brain. Here in lies the fact why these tumors are so hard to treat and patients usually have a poor prognosis. In the best centers in the world, we treat these tumors with a combination of surgery ( try to debulk the tumor and remove some of it and decrease the pressure in the brain), radiation (you may either radiate just the tumor or irradiate the entire brain to prevent metastatic spread) and chemotherapy. Radiation and chemotherapy may either be used concurrently  to supplement each other or one after the other. Again usually these tumor present at first with seizures and your doctor may start you on an anti-epileptic drug to prevent it.

I shall build on this discussion in my next post. Enjoy the weekend everyone, it is a beautiful day here in NYC.

Personal Regards,

Nitin Sethi, MD

Tremor: what is essential about it?

So let us discuss the diseases which can present with tremors.

1) Drug induced tremors: certain drugs can induce a tremor like I stated ealier. Drugs used to treat asthma (inhalers) and anti-epileptic drugs like valproic acid may induce a tremor in the hands.

2) Benign essential tremor: this as the name suggests is a benign tremor. Patients who have benign essential tremor usually have a postural tremor in their hands but may also have a head and speech tremor. They do not have any underlying neurodegenerative disorder and usually the tremor is not disabling and progressive. As the tremor is not disabling it may not need to be treated unless it causes social embrassement to the patient. Patients who have classical essential tremor notice that their tremor becomes less prominent if they consume alcohol (tremor is alcohol responsive).

3) Cerebellar tremor: patients who have cerebellar involvement (example if you have cerebellar tumor or diseases that involve the cerebellum such as multiple sclerosis) may also have a prominent kinetic (intentional) tremor.

4) Parkinson’s disease: patients who have Parkinson’s disease have a prominent resting tremor. This tremor is most prominent when their hands are at rest and becomes less prominent when they start to use their hands.

Treatment of tremors: like I mentioned earlier, not all tremors need to be treated. We usually treat tremors when they become disabling or socially embrassing to the patient. There are different classes of drugs that are effective for tremor of Parkinson’s disease, cerebellar tremor and essential tremor. Your doctor shall help in deciding what kind of medication may work the best for you. Sometimes if the tremor is particularly disabling and unresponsive to medication, it may respond to neurostimulation (deep brain stimulation). I shall discuss this in a separate post.

Dr. Sethi