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
I want to lay stress on the warning signs of a stroke. We all need to be aware of these as a stroke can strike anyone anywhere and with stroke time is brain. The sooner the stroke is recognized and help is sought the better is the outcome.
So let us get to the heart of the topic. The following are some of the warning signs of an impending stroke/ stroke in evolution:
1) Sudden onset of speech difficulty. Either unable to speak or unable to comprehend speech (the patient can speak but cannot understand, so whatever he speaks makes no sense. We call this jargon speech). At times the problem with language can be more subtle: unable to name things (we call this nominal aphasia or anomia), the speech is slurred (we call this dysarthia).
2) Sudden onset of weakness in one arm or leg usually of the same side. For example weakness in right arm and right leg or in the left arm and left leg. This weakness may be prominent and the patient may not be able to move the arm and leg at all or it may be more subtle.
3) Sudden onset of numbness in one arm or leg usually of the same side. Numbness is hard to define and patients may use words like “weakness”, “tightness”, “dead feeling” or “my one side feels as if I slept on it”.
4) Sudden onset of facial weakness. One side of the face usually starts to sag, the smile is crooked when the patient attempts to smile and the patient may drool from the angle of the mouth.
5) Sudden onset of gait problems: the patient is unsteady and falls when attempting to walk. The balance is off. Patient is clumpsy and appears “drunk”.
6) Sudden onset of visual problems: patient may have an episode of transient loss of vision in one eye ( I felt as if a curtain decended in front of my eye). We call this transient monocular blindness and this is a TIA (transient ischemic attack). Patients may also complain of a field cut (unable to see one part of the visual field).
7) Acute loss of hearing in one ear especially in the elderly (this is a rare sign of a stroke).
Nitin Sethi, MD
Continuing with the posts on the neurological manifestations of alcoholism, I shall cover the topic of alcoholic neuropathy here. Simply put alcohol is a neurotoxin especially when it is consumed in excess. People who consume large amounts of alcohol on a chronic (daily) basis frequently develop neuropathy. It does not depend upon the kind of alcohol consumed (top of the shelf Scotch whisky Vs a cheap rum) rather it depends upon the amount and frequency of use. Patients develop a predominantly sensory neuropathy and have complaints of pain, burning, tingling, pins and needle sensation in the feet and sometimes in the finger tips. Rarely if the neuropathy is severe patients may also develop peripheral weakness (motor symptoms).
Alcoholic neuropathy is also thought to be not entirely due to alcohol, rather it is a nutritional neuropathy and occurs due to lack of essential nutrients and vitamins in the marginal diets of alcoholics. It is uncertain whether the neuropathy would develop in an alcoholic who supplements his diet with essential nutrients and vitamins. Alcoholic neuropathy is more commonly seen in patients who have other neuropathic conditions like diabetes. In this subgroup of patients, alcohol acts as an additional neurotoxin and makes the neuropathy worse. The same principle applies to cancer patients been treated with neurotoxic chemotherapy medications or an HIV patient been treated with neurotoxic antiretroviral medications.
Thus the message is simple.
Drink alcohol in moderation applies to all of us.
People who have diabetes should avoid alcohol if possible or if that is not possible consume as little.
Patients been treated with neurotoxic medications should also avoid alcohol.
Supplement your diet with at least one to two tablets of a good multivitamin every day.
Alcoholic neuropathy is treated much the same as any other neuropathy (see my post on diabetic neuropathy http://braindiseases.info)
Nitin Sethi, MD
Let us discuss post-coital headache also at times referred to as orgasmic headache. What is post coital headache? The history is quite typical. This is a throbbing and at times intense headache which comes on at or near the height of orgasm. During coitus as sexual excitement increases, the muscles around the shoulder and neck become tense. There is increased blood flow to the brain and either at the height of the orgasm or soon after the patient complains of throbbing and at times intense holocranial (whole head) headache.
Post coital headache is relatively benign and does not warrant any urgent treatment. As the sexual excitement weans off, the headache too subsides and usually by the time the patient reaches the ER to seek care, the headache is subsiding or already gone. There is though one entity which can mimic a post coital headache in its clinical presentation and which warrants urgent evaluation. This is the headache which occurs when an aneurysm ruptures in the brain. Classically an aneurysmal headache is described by the patient as the ” worst headache of my life“. It is intense, holocranial, throbbing and accompanied by a stiff neck (as you can see the clinical presentation may resemble that of a post coital headache). An aneurysmal bleed though may be accompanied by other neurological signs and symptoms depending upon where the bleed has occurred in the brain and patients are usually obtunded by the time they reach the hospital. An aneurysmal bleed is a medical emergency and needs to be evaluated and treated urgently. Usually a special kind of scan is carried out to localize the site of the aneurysm and then either the aneurysm is coiled or clipped to secure it. I shall discuss the management of aneurysms in a separate post.
Nitin Sethi, MD
The human mind continues to fascinate me. Recently I met a close friend after a long time. Over dinner and drinks he filled me up on his life. He now had a successful business employing well over 20 people. As we were chatting he said Nitin, I feel I have a problem. I asked what, to which he replied “I think my brain is a confused mass of protoplasm”. Intrigued I asked what did he meant by that.
He answered ” my brain is always working. It never stops thinking. All the time I have thoughts going through my head. What I have to do today, what needs to be done tomorrow. How I wish for just a short while my brain would stop thinking. I am doing one thing but my brain is already thinking about what next has to be done. In the morning I get up to take a shower and as the cold water strikes my face, thoughts race through my mind. Needless and endless thoughts. Do you have any drug which I can take to control my mind?”
I guess the pressures and distractions of modern life has made all our minds (some more than others) confused masses of protoplasm. Our minds are constantly getting bombarded by external images, sense objects, pressures of modern life, all causing a sensory overload which our minds are unable to compensate for. More and more people are burning out at a young age, some willingly and others been forced to opt out of the rat race. Turning to meditation, yoga and solitude to bring this incessant brain chatter under their control. Unfortunately we still do not have any magic drug to switch on and off these thoughts and ramblings of the brain.
Till that happens we continue to suffer the price of modern existence.
Nitin Sethi, MD
I wanted to just touch on the subject of heat sensitivity in multiple sclerosis patients. MS patients are more sensitive to heat/ temperature as compared to non MS patients. It has been seen they do “poorly” whenever their body temperature is elevated. So when MS patients have fever, they become weaker and their neurological deficits become more prominent e.g. more blurring of vision, diplopia, ataxia and cerebellar dysfunction. Thus infections such as pneumonia and urinary tract infections (UTI) warrant to be aggressively treated with anti-pyretics and antibiotics.
Why does this occur? Well the thinking is that as the temperature of the body increases, it promotes cross-talk among the demyelinated axons and also leads to conduction blocks (block in the conduction of impulses in the neurons). This exacerbates preexisting neurological deficits.
So it follows that MS patients do better in colder environments as compared to warmer places. Better in winter as compared to the heat of summer. Keeping the ambient temperature of your house a few degrees below “normal” may be worthwhile though there is no scientific data to back this claim.
Nitin Sethi, MD
One of the most common type of seizures seen in the adult population is what are called complex partial seizures. As the name suggests these are partial seizures meaning that only a part of the brain has the seizure (remember in generalized seizures the whole brain has the seizure and hence the patient clinically has a convulsion, read my posts on epilepsy and seizures at http://braindiseases.info). Complex partial seizures differ from simple partial seizures. While in simple partial seizures there is no disturbance in the patient’s level of consciousness (the patient is awake and alert), in complex partial seizures there is an impairment in the level of consciousness. The patient may have his or her eyes open but usually is unable to respond or communicate. He may or may not comprehend if you try to speak to him during a seizure episode.
As many of the complex partial seizures arise from the temporal lobes in the brain, epilepsy of this kind is also referred to as temporal lobe epilepsy (TLE). That said and done complex partial seizures may also arise from the frontal lobes. Seizures arising from the frontal lobes can present with bizzare clinical manifestations, patient may become hyperactive during the seizure and have strange bicycling like movements of the legs. Complex partial seizures are at times associated with an aura. A simple way to define aura is what happens usually before the seizure. Prior to the onset of a seizure, the patient may experience gustatory or olfactory auras (smell of burning rubber, metallic taste in the mouth are the different classical auras mentioned in the textbooks of neurology). Other patients may mention they “feel wierd” or “dizzy”. Others mention a rising sensation in the stomach.
During the seizure apart from impairment in the level of consciousness, patients frequently exhibit what we refer to as automatisms. These are semi-purposeful movements. Examples include lip-smacking, chewing movements, tongue protusion, picking at the clothes (semi-purposeful movements of the hands). These patients may or may not have a “convulsion”. If the seizure spreads and becomes generalized then they go into a convulsion (such seizures are referred to as partial with secondary generalization).
If an adult presents with a new onset complex partial seizure, neuroimaging is warranted. This is because a new onset complex partial seizure raises the suspicion for an underlying structural lesion in the brain such as a cyst or a tumor (though I want to emphasize here that the most common cause of new onset seizures in the elderly is vascular, meaning a previous stroke).
Work-up for TLE includes an EEG, if needed a long term EEG recording (we call this a video-EEG study), imaging studies like CT scan (though the study of choice is what is called a MRI scan of the brain done under the epilepsy protocol). Thin slices are taken to look at the temporal lobes and hippocampus to make sure there is no structural lesion there nor is there any evidence for mesial temporal sclerosis (MTS).
There are many effective drugs for complex partial seizures/TLE. The most commonly used are carbamazepine (Tegretol) and oxcarbazepine (trileptal). If the seizures are refractory to medications, these patients can be worked up for epilepsy surgery (see my post on epilepsy surgery at http://braindiseases.info).
Nitin Sethi, MD
Is aging normal or abnormal/pathological? No one quite knows the answer to that question. What we do know is that as we age, neurological disorders become increasingly common. These may range from well defined neurodegenerative diseases like Alzheimers dementia, Parkinson disease and amyotophic lateral sclerosis to other less well defined conditions like gait disorders, “balance problems”, “forgetfulness and senior moments” and increased propensity to falls. Strokes become more common in the aged brain vessels.
As life expectancy increases and more and more people live past the eight decade, neurological conditions become common and account for substantial morbidity and mortality in the oldest old (above 85). Earlier when the life expectancy was in the 60s, we did not see so much Alzheimers dementia, Parkinson’s disease or brain tumors. People died of other “natural” and “unnatural” causes before the brain showed clinical manifestations of neurodegeneration.
Is it the norm that as we age, a substantial majority of us are destined to develop dementia? Clinical studies have clearly shown that Alzhemier disease pathology increases with age and the incidence of the disease becomes increasingly common as one goes past 85 (the oldest old). Other studies suggest that though not all the oldest old show clinical dementia, a substantial majority have cognitive difficulties if carefully tested for at the bedside.
Why do neurological conditions become more “common” as we age and can we do anything to alter this? Many theories have been propounded. Increased amyloid deposition in the brain has causal association with Alzheimers dementia, in the same vein deposition of iron in the basal ganglia has been postulated to cause various basal ganglia pathology. There is increased oxidative stress in the “aged” brain which leads to free radical formation and damage to the cellular DNA. Genes get switched off or on triggering the disease process. A lot still needs to be learned about the neurology of aging.
While the mechanisms are still been elucidated, is there anything which we can do to change our “risks”. In the absence of good studies most of the data is open to interpretation. Aspirin prophylaxis, modification of microvascular and macrovascular risk factors like hypertension, diabetes mellitis and dyslipidemia (high “bad” cholesterol) all seem to be reasonable interventions. Obesity and sedentary life styles are bad for the brain too. Regular physical as well as brain exercises (neurobics) keeps the brain healthy and increases neuronal reserve. The role of anti-oxidants like coenzyme Q10 and alpha lipoic acid is still been defined. As they are relatively innocuous and free from side-effects, I would recommend them on a case by case basis. Episodes of major depression “hurt” the brain and aggressive treatment with anti-depressants should be initiated early rather than late.
The neurology of aging remains an uncharted territory but there is hope yet.
Nitin Sethi, MD
Continuing with the effects of alcohol on the brain, in this post I shall dicuss a frequently asked question by people who consume alcohol, does it cause neurodegeneration? Does alcohol kill neurons/ brain cells?
Let us discuss the entity called alcoholic cerebellar and cerebral degeneration. We now sufficient data to suggest that excessive consumption of alcohol does damage the brain. Some parts of the brain are more specifically affected, these include the cerebellum. The cerebellum is the part of the brain which controls coordination, balance, gait as well has motor memory (memory for common motor actions performed by the brain). In the cerebellum are cells called the Purkinje cells which are selectively destroyed by alcohol ( the part of the cerebellum most commonly affected is the midline of the cerebellum between the two cerebellar hemispheres. This part is called the vermis of the cerebellum). So in alcoholic cerebellar degeneration we see vermian cerebellar atrophy in CT scan and MRI scans and also grossly if an autopsy is carried out).
So how does vermian atrophy present clinically?
Patients with alcoholic cerebellar degeneration have problems with gait and balance. Their coordination is off and they are prone to frequent falls (we have all seen the walk of a drunkard. While the clinical signs may not be so overt, on clinical examination we can usually pick up the signs of cerebellar dysfunction). Since these patients are prone to falls, they frequently land up in the ERs with head injuries (intracerebral hematoma, epidural and subdural hematoma). See my post on neurotrauma http://braindiseases.info).
Alcohol induced dementia: while this entity is not so well defined as alcoholic cerebellar degeneration, there is ample evidence to suggest that too much alcohol damages the cerebrum and can cause cognitive and memory problems. The thinking is that this is not entirely due to alcohol only. When someone abuses alcohol, he or she also does not consume a good diet and soon becomes deficient in essential nutrients and vitamins such as vitamin B12 and folic acid. So alcohol induced cerebral degeneration is likely due to nutritional deficiencies.
No one quite knows the answer that if you supplement your diet with vitamins and essential nutrients even in the face of heavy and chronic alcohol consumption, would that prevent the development of alcoholic cerebral and cerebellar degeration. Infact in certain countries of the world a plan was put forward to fortify all alcoholic beverages with vitamins and essential nutrients. One of the problems with this proposal is that it alters the taste of the alcohol. Your rum does not taste like rum anymore!!!
In any case I advise my patients to always drink in moderation and to take 1to 2 tablets of a good multivitamin every day apart from a wholesome and nutritious diet.
Nitin Sethi, MD
Let us talk here about a relatively common brain tumor called meningioma. I shall try to keep this simple yet cover some important aspects. Meningiomas are brain tumors which do not arise from the cells of the brain (as against glioms which arise from glial cells and other tumors which arise from neural cells). As they do not arise from “brain” cells, they actually are extra-axial in location. By that I mean, they are located outside the brain but inside the skull. So meningiomas do not actually “invade” the brain, on the other hand as they grow in size they press on the brain from outside inwards.
This is how meningiomas cause their effects. Depending upon which location the tumor is, as it grows in size it exerts pressure on surrounding structures. Pressure on the surface of the brain may cause seizures (so many patients may present with seizures and when a MRI scan is done the tumor is found), if they are near the optic nerve or tracts patient may present with slowly progressive loss of vision, if near the motor tracts with weakness in the arm and leg, if near the cerebellum with gait and balance problems.
Meningiomas are slow growing tumors and as I stated earlier they usually do not invade the brain (though they may be locally invasive at times and these tumors are called atypical or malignant meningiomas). As these are slow growing, if they are small in size and discovered accidently (as in you went for a MRI for some other reason and a meningioma is found but is not the cause of your symptoms), your doctor may decide not to do anything and just wait and watch and follow you with serial MRI scans. Frequently patients outlive their tumors and die of natural causes without the tumor ever becoming symptomatic. If for some reason it starts increasing in size and becomes symptomatic then a surgical option can be explored.
So now that we know something about these tumors, we can discuss how to treat them. The treatment option pursued depends upon the size and location of the tumor. If the tumor is the right size and in a surgically accessible location, then it is easy take it out surgically if it is symptomatic. However if the tumor is symptomatic but in a surgically inaccessible location like near the optic nerves then other options like sterotactic radiotherapy may be tried. The management decisions need expert opinion and hence one should consult a specialist.
Nitin Sethi, MD