Author: braindiseases

I am a qualified neurologist with sub specialization in the fields of epilepsy, clinical neurophysiology, sleep medicine and traumatic brain injury.

Disclaimer, privacy concerns and more

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Please read my disclaimer which I have posted at multiple times throughout the year. Also again I strongly urge you not to post comments with your true names and other data which can identify you. Health information is private and should remain so.

The blog remains free of any commercial interests. I had started it as a means of disseminating information about neurological diseases to the public at large. I am happy to report that after 4 years,  the goal of my blog and website (http://braindiseases.info) remains unchanged. There are no financial incentives and the two projects remain a solo effort on my part.

Thank you for your continued support.

 

Nitin Sethi, MD

Brain diseases blog: it is up and running again

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To the readers of my blog and my website (http://braindiseases.info) thank you for your continued support and positive feedback as well as constructive criticism.  I apologize for my delay in replying to your questions. No good excuse apart from that I was really busy the last few months. The blog though is now up and running and I shall be answering all your questions as well writing a few new posts.

Personal Regards,

Nitin Sethi, MD

Side-effects associated with anticonvulsant use

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Anticonvulsants (anti seizure medications) use is associated with various side-effects. Some of these can be troublesome. In this post I shall briefly list a few of the side-effects common to a number of anticonvulsants. As always my advise remains unchanged. The information provided here is no substitute to an actual visit to your physician. But I hope this post shall make you better informed.

Rash: can be associated with the use of a number of anticonvulsants. Phenytoin, lamotrigine, carabamazepine are the anticonvulsants commonly associated with rash. The rash may be mild or it may become quite fulminant leading to involvement of the mucous membranes (Steven Johnson Syndrome). The rash usually appears right at the onset (meaning a few days after the medication is started) but it may also appear at any point of time during the course of therapy. If rash is documented the usual advise is to stop the medication and consult your physician as soon as possible. Please remember though that sudden stoppage of anticonvulsant is not advisable since it may lead to a flurry of seizures. So it is your doctor who shall be the best person to make the decision: either stopping the medication cold turkey and substituting another anticonvulsant in its place  or slowing down the upward taper of the anticonvulsant and allowing the rash to subside.

Cognitive side-effects: a number of anticonvulsants can cause cognitive side-effects. Patients may complain of feeling dull (“I do not feel as sharp as usual” or “my mind is in a fog”). Some complain of difficulty concentrating and focusing while others have word finding difficulty (has been reported with the use of topiramate). Again if you experience any of these side-effects bring them to the attention of your doctor. At times lowering the dose of the anticonvulsant leads to resolution of these side-effects. At times taking the bulk of the anticonvulsant at night (larger dose at night and smaller dose in the morning) may be helpful since you can sleep off most of the side-effects.

Bone loss: many anticonvulsants lead to bone loss. The most commonly cited culprit drugs are phenytoin, carbamazepine and phenobarbital. Prolonged use of these anticonvulsants leads to bone loss and osteoporosis. That is the reason why your physician may advise you to supplement calcium and vitamin D. How much calcium and vitamin D to take on a daily basis though? The National Osteoporosis Foundation and National Institute of Health has given recommendations for daily calcium and vitamin D intake and most of the physicians refer to these.  Again your physician shall be the best person to determine how much calcium and vitamin D supplementation is required based on your age, the various medications you are taking and your risk of osteoporosis in the future. He may refer you for a bone densitometry test (commonly referred to as a DEXA scan).

Congenital malformations (major and minor): this applies to women of child bearing age who are exposed to/ taking anticonvulsants. Data from various pregnancy registries collected over many years has now informed us that anticonvulsant use by a woman during pregnancy may at times lead to major or minor malformations (cleft lip, cleft palate, congenital heart disease, spina bifida and so forth) in the baby. The risk though varies with some anticonvulsants “safer” than others.  No anticonvulsant though is completely free of this risk and again it is your doctor who shall be the best person to advise you about this.  The choice of an anticonvulsant in a woman of child bearing age is made after due consideration of the above risk. Folic acid supplementation before and during pregnancy may help to mitigate some of this risk to some extent.  So it is imperative that all women of child bearing age who are on anticonvulsants (and are contemplating pregnancy) should have a discussion about the risk of congenital malformations with their doctors.

Mood changes: anticonvulsants can lead to mood changes. Studies have shown that some are more likely to do so than others. Patients may complain of low mood, caregivers may notice that the patient is more agitated, snappy or restless. Some patients may become depressed. Hence the FDA has issued a warning on anticonvulsants and the risk of suicide and suicidal thoughts. Again your physician shall be the best person to decide which anticonvulsant is appropriate for you.

Apart from the above mentioned side-effects, each anticonvulsant has side-effects which are unique to it.  So it is important that you read the package insert and tell your doctor about any other medical conditions that you may have. Also mention other medications that you taking so that your doctor can determine and tell you about important drug-drug interactions.

I hope this information helps some of the readers of my blog.

 

Nitin Sethi, MD

Disclaimer

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This blog is my own endeavor and project. Though I work in New York-Presbyterian Hospital, Weill Cornell Medical Center, New York, the blog is in no way connected to the hospital.

The information provided in this blog should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 if you have a medical emergency.

Links to other sites are provided for information only — they do not constitute my endorsements of those  sites.

 Any duplication or distribution of the information contained herein is strictly prohibited.

 

 

Nitin Sethi, MD

Disclaimer

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Please do read the disclaimer I have posted on my blog. Also to all my readers, if you do decide to write in to me or to post on this blog–do so but remove all identification features. Remember medical information is private and should remain private.

Trigeminal Neuralgia: ouch that hurts!

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I recently saw a patient with trigeminal neuralgia. She was in severe pain when she walked in to see me. Trigeminal neuralgia is the condition we shall discuss in today’s post. In the tradition of this blog, I shall keep things simple and free of medical jargon.

So what is trigeminal neuralgia and how does the patient present? As the name suggests trigeminal neuralgia is basically pain in the distribution of the trigeminal nerve. The trigeminal nerve is a cranial nerve which supplies the skin of the face (so when I touch you on the forehead or on your cheek, you are able to appreciate that touch basically on account of the trigeminal nerve). Every nerve starts from somewhere and ends somewhere. In the case of the trigeminal nerve, the nerve originates in the brain (brainstem area) and then courses inside the brain/skull for a while before it exits out and supplies the skin of the face. The nerve also has a motor branch which innervates the muscles of mastication (which help in chweing function). Now if the nerve is compressed/pinched somewhere along its course (usually occurs near the origin of the nerve in the brainstem), it gives rise to a particularly painful and distressing condition which is called trigeminal neuralgia.

Patients with trigeminal neuralgia present with pain. The pain has been described as shooting, stabbing, brief electrical shock like sensations that radiate down into the face. Usually the history is typical. The pain is triggered by touching the face as what happens when the patient attempts to shave or brush his teeth. Sometimes even a gust of wind may trigger the paroxysm of pain. The pain does not respond to conventional pain killers such as ibuprofen (Advil or Motrin) and even stronger pain killers such as codeine and this results in a visit to a doctor.

Frequently the diagnosis may be delayed and the patient may initially consult a dentist since it is wrongly assumed that the pain is dental pain. Patients have undergone root canal and tooth extraction only to realise that the pain was not dental to begin with.

So what causes trigeminal neuralgia? Well the cause usually varies with age. Idiopathic trigeminal neuralgia usually occurs in the older age group. In these patients a MRI of the brain may reveal no gross abnormality (aka there is no obvious tumor found). The thinking behind idiopathic trigeminal neuralgia is that the nerve gets pinched by a tortuous blood vessel. As we grow old our blood vessels (including those inside the brain) become tortuous and thickened. A tortuous artery may press on the delicate trigeminal nerve in the brainstem giving rise to the pain of trigeminal neuralgia. When trigeminal neuralgia occurs in a young person other things need to be ruled out. Is there a tumor in the brainstem pressing on the nerve? Does the patient have multiple sclerosis (a young lady presenting with trigeminal neuralgia is the typical example. In such patients the multiple sclerosis lesion/ plaque is the culprit and presses on the nerve near its origin).

So now lets talk about management. There are two aspects to this. Firstly the cause of trigeminal neuralgia needs to be determined. Your doctor shall order a MRI scan of the brain with and without contrast with close attention at the trigeminal nerve. The idea is to find the culprit blood vessel which is pressing on the nerve and to rule out other lesions such as multiple sclerosis plaque or a small brainstem tumor. Simultaneously the pain has to be addressed. The pain does not respond to conventional pain killers but may respond to medications which are effective for neuropathic pain such as carbamazepine (Tegretol), oxcarbazepine (Trileptal), gabapentin (Neurontin). Other medications which may work include baclofen and amitriptyline (Elavil). My personal experience has been that the pain responds to carbamazepine but high doses are frequently needed. If pain relief is inadequate, I add low dose baclofen.

If the pain subsides well and good. At times I shall only keep the patient under observation and do nothing more (this of course applies to patients who have idiopathic trigeminal neuralgia).  If there is a tumor that is pressing on the nerve then that of course needs to be addressed. If the cause is multiple sclerosis then multiple sclerosis needs to be addressed. There are other options available. Namely:

 

Surgery–the surgery is called microvascular decompression. As the name suggests the idea is to decompress the nerve. The neurosurgeon shall expose the nerve and identify the blood vessel pressing on it. The vessel is then lifted off the nerve thus decompressing the nerve and providing long lasting pain relief. The surgery is not simple. It requires the expertise of a neurosurgeon trained in this procedure. As the trigeminal nerve is hidden deep in the brain, it takes sometime to expose the nerve. Another procedure which is becoming more popular nowdays is radiosurgery. Several reports have documented the efficacy of Gamma Knife‚ stereotactic radiosurgery for trigeminal neuralgia. This though is available only in some centers around the country. Percutaneous procedures are also available. They bascially involve injecting the trigeminal nerve ganglion with chemicals such as glycerol. The idea is to kill the nerve and hence abolish the pain.

I hope some of you find this post helpful.

 

 

Nitin Sethi, MD

Alcohol and seizures: a few questions and their answers.

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One of the readers of my blog asked me a few questions. His questions and my answers to them follow.

Hello Dr Sethi! To begin with, I’d like to thank you for clarifying and educate us about seizures.(esp. rum fits, alcohol withdrawal seizures and Dts seizures)

I have some questions:

1. How would I differentiate between epilepsy and alcoholic fits? Ignoring any test(EEG,CT), i mean based on the clinical manifestation?eg. duration of fits?the sequence of occurence (pattern of seizure)?etc…

2. how would i differentiate between epilepsy and the ‘fits’ that is seen in patients with hysteria (conversion disorder)?

3. is treatment necessary for alcohol fits? or just allow the patient to relax in the recovery position and let the fit go away?

4. how would you distinguish between: alcohol withdrawal syndrome and DT? is there any special cardinal symptom that will give me a clue that the patient is in DT.?

Thank you very much Dr Sethi. looking forward to hear from you.

Dr. Ronny Gooriah (doing Internship)

Dear Dr. Gooriah,
thank you for writing in to me. I am glad you found the information presented useful. Now without further delay, let me answer your questions.

1. If I understood your question you want to know how to differentiate between seizures caused by alcohol (alcohol fits) from seizures/epilepsy caused by other conditions. As you may be well aware of, epilepsy is a condition which predisposes the patient to multiple convulsions in his/her lifetime. There are numerous causes of epilepsy. Broadly speaking epilepsy can be idiopathic , symptomatic or cryptogenic. Seizures may also occur secondary to a medical condition which may or may not involve the brain like for example a brain tumor, head trauma, meningitis or encephalitis and in the setting of multiorgan failure such as sepsis, renal or hepatic failure. There is no absolute way of differentiating a seizure caused by alcohol (excessive use or sudden stoppage) from epilepsy (whether idiopathic, symptomatic or cryptogenic) specially early in the course of the disease. One needs to take a thorough history which should include a history of alcohol intake. How much? what kind? over what time frame were the drinks consumed? were drinks mixed? were recreational drugs taken along with the alcohol and so forth. Other history which may be helpful in determining if the patient has epilepsy include: a history of febrile convulsions, family history of seizures, history of meningitis or encephalitis, history of significant head trauma and if seizures have occured in settings where the patient was not abusing alcohol. The answer to all these questions and the results of tests such as EEG and neuroimaging (MRI brain) shall help in determining whether the patient has epilepsy per se or whether all his seizures can be attributed to alcohol.

2. Nonepileptic events (pseudoseizures) may occur as a manifestation of a somatoform or conversion disorder. These patients have events that look like seizures (sudden shaking of the body and the patient may appear to suffer loss of consciousness) but there is no EEG correlate to these events. Meaning that the EEG shows the patient is not having a seizure. Patients who exhibit nonepileptic events (some doctors refer to them as hysterical convulsions) usually fall in two categories. Either they are doing this for a secondary gain (seeking attention, disability or financial compensation aka they are malingering) or these events are really not under their conscious control (usually these patients are under severe mental stress or may have history of physical or sexual abuse). A trained eye (such as a neurologist) simply by looking at the clinical event shall at times be able to determine if it is a true seizure or a pseudoseizure/ hysterical convulsion. At times though the differentiation is indeed difficult (if solely based on the description of the event). A video-EEG in these cases is extremely helpful. As the name suggests the patient is attached to a EEG machine while under video surveillance. The idea is to capture a typical seizure on the camera and look at the EEG at the same time.

3. If the patient suffers a single alcohol related seizure, no treatment may be necessary apart from simple observation and making sure the patient does not hurt himself. On the other hand if the patient suffers a flurry of seizures one after the other, you may have to give medications to stop the seizures at least acutely. Whether such patients warrant long term anticonvulsant therapy is another issue and needs careful consideration.

4. Patients who are in DT or have impending DT usually have dysautonomia. They are frequently tachycardic or have irregular heart rate, their blood pressure may be high and have wide swings, they may have profuse sweating and are disoriented, confused and agitated (hence the word delirium). DT has a high mortality and hence these patients need close supervision and aggressive treatment usually in an intensive care setting.

I hope I have answered your questions to your satisfaction.

Personal Regards,

Nitin Sethi, MD

Seizures: a question and an answer

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One of the readers of my blog wrote to me recently. His question and my reply to it follows. I think some of you may find it helpful.

 

Hello Dr. Sethi,
 
I came to your site/blog while doing a Google search regarding delirium tremens, which I found extremely helpful!  So I thought I would ask for your opinion about a diagnosis my neurologist gave to me about half a year or so ago.  Please feel free to remove my email and name and post on your blog!
 
So my history is that I’m 20 years of age and have had two seizures in the past…36 months or so.  I have had no family history of seizures or epilepsy, one case each of diabetes (treated with metformin), stroke (no known treatment), and breast cancer (treated by partial mastectomy).  Both sides of my family are on high blood pressure medications.  I myself have a history of reactive airway disease.  I have also been prescribed lots of co-actifed and have developed a bit of an addiction to using drugs that cause sedation; among the things I can list are: codeine, diphenhydramine, Actifed, lorazepam, and tramadol (I would say this is probably significant), and I often self dose; with high amounts of codeine, and often double or triple the recommended doses for benadryl and Actifed (as on the box); these three are the most common drugs I take to sleep, I realize I am developing a tolerance to them.  I am trying to stop using these as a way of falling asleep. 
 
Anyway, so the first incidence of my seizure happened when I was working on my computer, writing up a laboratory report that I was working on for a while.  I had been sitting there for several hours already.  I had been taking tramadol on and off for the couple of months or so.  I fell into a seizure and my mother found me.  Nobody saw what happened as I slipped into a seizure, I just fell backwards. 
Key things I remembered/observed:
-I did not have an aura
-I did not have incontinence
-I instinctively bit down, but I do not know if I bit my tongue because my mom had put her finger in my mouth
-I had nausea when I woke up
-The whole sequence of events I believe lasted around 5 or so minutes. 
 
The ER doc and the paramedics had concluded the seizure was due to tramadol. 
 
The second incidence of seizure happened when I was sleep deprived, though arguably I was sleep deprived in the first incidence too.  I had only slept several hours the night before and I did not nap (which I usually do for several hours during the day).  I spent the whole day awake, and I went to a friend’s house afterwards.  I was playing a poker game, which often makes me feel really stressed (I get sweaty palms, feeling of coldness, a bit of light-headedness, and sometimes I get slight dizziness).  I remember that I had not eaten much at dinnertime and I was hungry, so I ate a bunch of chips as a snack, with an iced tea to drink.  I remember I had slipped into a seizure, again with the same symptoms as the first time, lasting about 5 minutes.  The key issue is that I did NOT bite my tongue. 
 
Again, I was taken to the ER and the ER doc was not sure what could have caused it.  I do not recall taking any drugs throughout the course of the day but I might have taken some diphenhydramine to sleep the night before.  I realize that these act on the nervous system.  The ER doc immediately prescribed me phenytoin and referred me to a neurologist, and an EEG ordered. My neurologist subsequently ordered an MRI.
 
 
When I went to see my neurologist, she examined me as usual and asked for the same details I have given above.  Her conclusion given her initial diagnosis was an epileptic seizure of cause unknown.  Her suspected trigger was sleep deprivation.  A second neurologist I visited repeated the diagnosis. 
 
Following the EEG and MRI, I went back to see my neurologist (this was after several visits).  The EEG had come back normal.  I did not lose consciousness (aside from the sleeping phase of the test) nor was ever informed that I had a seizure during the course of the test.  The MRI had also come back as negative in anything in my brain.  I was not informed of any other explanation other than a “possible” epilepsy condition.  Neurologist placed me on phenytoin, which I took for three weeks before having an allergic reaction and had to be switched over to levetiracetam.  Following that I saw the neurologist again due to severe depression and mood disorder.  We decided mutually not to take the medication, of which she warned me that there was a 75% chance of a third seizure in the following year. 
 
To this date, I have not had another seizure, and about 7 months has passed since the incident.  Again I have not taken any antiepileptics aside from occasional (several days to several weeks in between doses) lorazepam 1mg. 
 
I should note also that while having taken lorazepam 1mg-2mg (and being off of it for a week), I have subsequently drank more alcohol than I usually do and taken a ranitidine 150mg before going to drink (supposedly to prevent hangovers and being able to drink more).  The amount I drank was about 2 shots and a beer, before I started to experience delirium tremens.  The odd thing is, however, that exactly one week after that incident, I drank the same amount of alcohol but did not have delirium tremens (without having taken the ranitidine).  I understand how alcohol works in the brain by depressing the nervous system. 
 
I understand that the medication is preventative, but I am worried that I might have another seizure.  It puzzles me since my lack of taking medication should therefore result in seizures if I really have epilepsy.  I understand that drugs can cause seizures, especially in overdosing amounts, however, I would really like a second opinion about whether or not I really do have epilepsy.  Of course I understand that your opinion is only an opinion since I have not been examined by yourself, but I have provided as much relevant information as I can.  I also understand that there are many triggers of epilepsy, and often the cause isn’t really clear.  I would like to be seizure free of course and not have to take medication, but my neurologists are telling me otherwise, which concerns me. 
 
Please reply to me with your opinion as your time allows.  Oh please feel free to also use medical jargon if you wish in your replies, I am actually studying as a pre-med student myself, which might be where the stress is coming from. 
 
With Regards and thanks,
 
xx
Dear XX,
                               thank you for writing in to me. You gave me a very detailed and thorough history. While as a rule I do not and should not diagnose someone over the Internet since I have neither taken the history myself nor examined them, I do have a few words of advice. It is likely you have an underlying tendency to have a seizure. It is also well known that sleep deprivation, excessive use of over the counter antihistamincs and other prescribed medications such as lorazepam, codeine and Tramadol can lower the seizure threshold especially when you are mixing these medications with alcohol.
 
Let me explain in another way. Two of your doctors (ER physician and neurologist) feel that you have epilepsy and prescribed anti-convulsant therapy. A normal EEG and a normal MRI brain do not rule out epilepsy. Infact many epileptics may have a normal routine (40 minutes) EEG study. Hence to increase the yield sometimes a more prolonged EEG study is ordered (such as a 24 hour ambulatory EEG study or an inpatient video-EEG study). If the EEG study clearly shows interictal epileptiform discharges, it strengthens the argument that you suffer from epilepsy and that it shall be prudent to continue taking an anti-convulsant since the chance of a third seizure is high. On the other hand if the EEG study comes back normal, we are back to square one. It does NOT rule out epilepsy. Levetiracetam has been reported to cause psychogenic side-effects such as anxiety. It can also make patients frankly depressed. So a mutual decision between you and your physician was made to stop levetiracetam.
 
If I understand your email right, at present you are NOT on any anti-convulsant therapy. Your physician rightly informed you of the risks of taking this approach. You should remain in close follow up with your neurologist. Also since you have already suffered two convulsions (and have decided not to continue anti-convulsant therapy), it shall indeed be prudent if you make significant lifestyle changes. Namely avoiding alcohol completely or if that is not possible drinking in extreme moderation. I would also advice cutting down your use of over the counter sedatives, antihistaminics and other sleeping aids. You should maintain seizure and fall precautions at all times. Remember seizures are associated with falls and sometimes fatal injuries have occured. I always tell my patients  “you do not want to have a seizure at the wrong place and at the wrong time”. You should not drive as per the law of the state you reside in. Maintain good sleep hygiene and again remain in follow up with your physician. He/she shall be the best person to guide your care going forward.
 
Personal Regards,

Nitin Sethi, MD

Neurology should be fun!!!!

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A letter from Sister Lazarus

Hi, Doc. I wanted to thank you for putting your site together. It is very helpful to have plain English explanations of neurological terminology. I have been referred to a neurologist because I have foot-drop in my right foot and am beginning to have episodes of foot-drop in my left foot. All of my doctors have been unable to elicit any reflexes from my upper or lower body. They hit me and nothing happens then they hit me again and nothing happens. Then they ask me to clench my jaw as they hit me and nothing happens. Then they make me sit in odd positions and hit me. And, yup, nothing happens. What on earth are they looking for? I think they think I am a bit mad because after a while I just can’t help laughing at them. Whacking people with hammers is like being in the Stone Age or something. In my imagination I can see a dinosaur sitting in a hospital gown on an examination couch and a doctor has just come out from  behind a curtain weighing an enormous stone club in his hands and he’s saying, ‘if this doesn’t get a response nothing will…’ and the dinosaur’s eyebrows are up off his forehead — like a Far Side Cartoon. I don’t know, it just strikes me as very, very funny, especially when the same doctors then send me off for space age scans in MRI machines. It is so weird – blunt instruments and quantum mechanics all in the same day. Neurologists are a breed apart. I don’t know if you know how strange you are…? I mean that in the nicest possible way 😉

Anyway, would you please put a page together for your website explaining what the doctors are looking for when they whack their patients with hammers and what it means when they get or don’t get a reaction? I would appreciate it (and I think other patients would too).

With many thanks,

All best wishes,

Sister Lazarus

 
 
 
 
Dear Sister Lazarus,
                                   thank you for your kind email. It brought a smile to my face. I shall certainly put up your post on my website (with your permission I hope) and shall help explain the mystery behind eliciting deep tendon reflexes with the use of a reflex hammer. May I tell you something. I have noticed that even my most serious/ tough patient shall break into a smile or a giggle when I tap on their reflexes. Maybe for that reason itself I shall keep the mystery of the reflex hammer a mystery.
 
Personal Regards,
 

Nitin Sethi, MD

Alcohol and seizures: a question and an answer

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T

HI
My Father is an aolcoholic and last Sept he was admitted to hospital after a fall when drunk – whilst in hospital he had a fit – understandable he was cold turkey whilst there. He was treated and sent home. Since Dec he has reduced his drinking and now generally consistantly drinks 1 bottle red wine a day – yes this is still too much but about 50% what he used to drink – he reduced gradually and has maintained this intake for a few months now.
What I find strange is that all i can find about these alcohol withdrawl fits relates to 2-3 days without alcohol – Dad had a fit a few mornings ago after a normal day and normal alcohol consumption levels. The hospital saw alcohol in his notes and packed him off home again with some Vitamin B tablets.
How many alcoholics normally get fits whilst they are still drinking? How normal is this? He is eating better these days than he was but still could do with eating more. He borderline underweight and 74 years old – he has been dependant for more years than I can imagine but probably the last 12 years have been the worst. He does not drink in the morning but the first drink in the day is normally 3/4pm and last drink 6/7pm before bed. This one bottle of wine is often enough for him to fall when on his way to bed or even a few hours later I have had to carry him back to bed if he falls in the bathroom. His body just doesnt seem to be able to cope with alcohol any more – less alcohol to get drunk – is this why he is having the fits?
My apologies for long winded questions but the question needed some context to make sense I think. Any I am not delusional about his alcohol intake – I monitor it and he has no other way or place to stash any.

Thank you so much in advance

P.S. the fit was 6.30 am Thursday and now Sat pm he is still very unsteady and his memory is worse than before. What is the normal recovery from these fits?

 

Braindiseases

Dear T,
thank you for writing in to me about your father. There is no one set limit above which alcohol can induce a seizure. The limit varies from person to person. Rum fits (seizures which occur at the height of binging) of course occur when one consumes too much alcohol in too short time. Alcohol withdrawal seizures classically occur 24-48 hours after the last drink (they occur in people who are chronic alcoholics/ people who consume heavy alcohol on a daily basis and who then suddenly stop drinking). Again not every chronic heavy drinker gets alcohol withdrawal seizure if he/she stops drinking suddenly. Usually it is the person who is chronically malnourished and dehydrated who is more predisposed to an alcohol withdrawal seizure in the setting of sudden cessation of drinking. These people as you can well imagine are deficient in multiple vitamins and minerals (commonly the B group of vitamins such as Vitamin B1, B2, B6, folic acid and B12). Their electrolytes are also more likely to be off (meaning they serum sodium, potassium, magnesium is low). They may also have alcoholic liver disease (alcoholic steatosis or fatty liver, alcoholic hepatitis and finally cirrhosis). During their prolonged drinking years they may also fallen down and struck their head. So it is a combination of factors (meaning the overall health status) and not just the sudden cessation of drinking which predisposes some alcoholics to alcohol withdrawal seizures.
Finally over the course of years of heavy drinking, some alcoholics develop epilepsy. The reason for this may be any of the above I have listed. My personal feeling is that these patients likely have underlying epilepsy and alcohol (in excess or sudden cessation after years of drinking) just helps to unmask it.
Now let me answer your last question about time frame of recovery. Again if his pre-existing neurological status is compromised (his memory is already bad after years of drinking, his general medical condition is poor or if he has coexisting medical problems such as chronic lung or liver disease, diabetes or congestive heart failure) his recovery from a convulsion shall be slow as compared to a young person with no pre-existing medical problems.
I hope I have addressed some of your concerns. I wish you both my very best.

Personal Regards,

Nitin Sethi, MD