Urinary incontinence occurs when a person loses his/her control over the urinary bladder resulting in involuntary leaking of urine. In addition to being a disease condition it is also associated with social stigmas.

Anatomical issues

The urine is formed in the kidneys and reaches the urinary bladder through a pair of tubes called as ureters. The urine from the bladder is emptied through another tube like structure called urethra. There are two muscular sphincters (gates) where the bladder joins the urethra; an inner involuntary and outer voluntary and both regulate the emptying of bladder. Prostate is a glandular structure seen only in men and the pelvic portion of urethra passes through it.

Types of incontinence

The major types of incontinence are;

• Stress incontinence
• Urge incontinence
• Overflow incontinence
• Mixed incontinence (stress & urge types together)

Stress incontinence occurs whenever there is increased stress or pressure in the pelvic and/or abdominal cavities forcing urine to leak out, e.g. during weight lifting, coughing, sneezing, bending etc.

Urge incontinence occurs when urinary bladder becomes over sensitive to its filling and creates an abnormal urge to void urine however urine leaks out generally before you reach bathroom.

Overflow incontinence occurs when urine fills to its capacity, however for certain reasons the person cannot void immediately, and since the bladder has filled to its maximal capacity leakage is the only way to make room for additional urine filling the bladder.

What actually causes incontinence?

Stress incontinence:

Normal people while executing above mentioned strenuous activities do not experience incontinence. Imagine how much weight an Olympic medalist has to lift, if incontinence results then such events like weight lifting etc would have been excluded from such athletic meets.

Luckily our pelvic cavity is endowed with a very effective mechanism in the form of powerful muscles and connective tissues that withstand an enormous pressure and prevent any inadvertent bladder leakage. If damage occurs to these structures due to any prior surgeries, infections, child birth injuries, traumas etc can precipitate stress incontinence.

Urge incontinence:

Urge to empty the bladder is a normal phenomenon to start with. As the bladder starts filling this urge gradually builds and progresses in parallel to the amount of urine filled. A normal person has a lot of control on when to initiate the urination e.g. if you are in the middle of doing something you can delay the emptying.

For patients with this type of incontinence there is an exaggerated urge to empty the bladder and many times the urge is so strong that the patient cannot inhibit this impulse. So the person has to rush to the bathroom immediately or urine leakage can occur wherever they are.

Urge incontinence is seen in the following settings including;

• Idiopathic overactive bladder (cause is not found)
• A small & spastic bladder (due to stroke, spinal cord injuries etc)
• Bladder infections
• Bladder stones etc

Overflow incontinence:

Normally people should be able to void their bladder before it overfills and starts leaking, so any situation or health condition where people cannot accomplish their bladder emptying on time will experience this type of incontinence.

The clinical profiles of patients who experience this type of incontinence include;

• Non ambulatory ones due to any health conditions and cannot reach the toilet in time
• Demented or confused ones that cannot tend to their body’s demands and urges
• Benign prostate hypertrophy
• Those not able to feel their bladder filling etc.

There are neurological conditions where the patients are not aware of the filling of their bladder. The sensation of filling of bladder is carried to the awareness centers in the brain through nerve fibers in the pelvis and then through ascending fibers in the spinal cord and brain. If there is discontinuity anywhere along this awareness pathway then the patient may not initiate emptying the bladder (not their fault!) so eventually when it overflows it forces opening of the sphincters of urethra and results in incontinence but of course it is a safety measure as if this doesn’t happen bladder might rupture open.

Diagnosis

After the clinical evaluation your doctor will mostly order one or more of these tests including;

• Urine analysis (detailed)
• Blood tests
• Uro-dynamic studies
• Neurological investigations (CT/MRI, EMG, spinal tap etc)
• Prostate evaluation etc.

Management

There are neurological, obstetric/ gynecological, surgical, psychological, general medical causes for incontinence. If cause is specifically related with one particular specialty then they will generally manage the problem. However sometimes the cause for incontinence is not clear so several specialties will work in unison to resolve the issue.

If a specific cause is detected then it is treated as follows;

• Urinary tract infection is treated with antibiotics
• Bladder stone is treated appropriately (fluid therapy, surgeries etc)
• Benign prostate hypertrophy is managed with medications or surgery
• Prolapsed uterus treated with hysterectomy
• Neurological causes like strokes, multiple sclerosis are treated appropriately

Other measures include;

• Medications like oxybutinin, tolterodine etc (especially for urge incontinence)
• Scheduled bladder emptying
• Intermittent bladder catheterization
• Bladder exercises
• Fluid restriction
• Avoiding or reducing caffeine intake etc.

Syncope or fainting is a relatively common health condition and is characterized by a sudden and often temporary loss of consciousness secondary to decreased nutritional supply to the brain like oxygen, glucose etc.

Majority of times syncope results due to a reduction in blood supply to the brain which automatically deprives the brain of the above mentioned nutrients, however sometimes blood supply is adequate but the severe deficiency of a particular nutrient in the blood like hypoglycemia (low blood glucose) is what causes it.

Types & Causes

Broadly the syncope can be categorized as;

• Cardiac (heart related) &
• Non cardiac

This initial categorization is of vital importance as experience has shown that cardiac syncope is associated with increased risk of death while the other types generally not.

Causes of cardiac syncope include;

• Obstructive lesions like aortic or mitral valve stenosis
• Irregular hear beats (or cardiac arrhythmias)
• CHF (congestive heart failure) etc.

Causes or types of non-cardiac syncope include;

• Reflex or neurally mediated
• Other causes (e.g. postural hypotension, hypoglycemic syncope etc)

The reflex or neurally mediated type is further grouped as;

• Vasovagal syncope
• Situational syncope (e.g. while swallowing, urinating, defecating, shaving etc)

The reflex or neurally mediated syncope is generally more frequent in young adults while the cardiac causes and postural hypotension are more frequent in older people.

How syncope results?

For cardiac syncope, irrespective of the cause the common immediate precursor to fainting is reduced cardiac out put. Diminished cardiac out put deprives the brain of its nutrients and results in syncope. There are myriad cardiac causes including few of them mentioned above and some more causes include;

• Sick-sinus syndrome
• Adams-stoke’s syndrome
• Cardio-myopathies
• Dissection of aorta etc.

Vasovagal syncope results from a seemingly complex neural mechanism that involves activation of so called ‘vasodepressor’ mechanism, which promotes abnormal pooling of blood in the peripheral vessels and diminished cardiac out put and this suppresses the brain perfusion and results in syncope.

Situational syncope is similar to vasovagal type except for an individual patient the syncope is coupled with a particular situation like;

• Deglutition syncope (while swallowing)
• Mictuirition syncope (while urinating)
• Defecation syncope (while passing bowels)
• Cough syncope (while coughing) etc.

Carotid sinus syncope is also an example of this group. Carotid sinus is a dilated proximal portion of an artery called internal carotid artery that supplies brain and is located in the neck. A pressure on this region can activate the vasodepressor mechanism and induce syncope. Wearing a tight collar, neck tie, or during shaving or massage of this region all can induce fainting.

Postural hypotension may be caused when patient is dehydrated, or on medications or has neuropathies (nerve damage) that cause the dilatation of blood vessels in the legs promoting abnormal pooling of blood resulting in decreased cardiac out put.

Clinical Manifestations

The episode of passing out is usually preceded by one or more of these symptoms;

• Dizziness
• Blurring of vision
• Feeling your heart beats
• sweating
• Cold & clammy feeling
• Nausea
• Vomiting
• Convulsive syncope (brief convulsive movements in few patients but not true fits)

Diagnosis

Although the clinical diagnosis of syncope is relatively straightforward however establishing the causative factor is not always easy. Myriad health conditions may present with syncope as one of their symptoms and additional laboratory investigations are necessary, the following is a bunch of tests ordered although not every patient will require each and every one in this list.

* Serum electrolytes
* Blood cell counts
* Heart enzymes
* ECG
* Holter monitor
* Stress test
* Echocardiogram
* CT (CAT) Scan of brain
* MRI of brain
* EEG
* Carotid ultrasound
* MRA (magnetic resonance angiography)
* Carotid sinus massage
* Tilt table test etc.

Serum electrolytes test will detect any lower blood glucose, sodium etc causing syncope. Cell count will mainly look for anemia as the cause. Heart enzymes, ECG, Holter, echocardiogram are tests to evaluate the functioning of the heart. They will rule out conditions like heart attach, irregular heart beats, valvular pathologies predisposing to syncope. CT or MRI of brain will rule out any structural brain pathologies; carotid ultrasound & MRA will look for any vascular narrowing as a cause for syncope. EEG will try to establish whether the episode was seizure rather than syncope. A tilt table test is another useful test for the evaluation of especially vasovagal syncope. Carotid sinus massage is a risky procedure but helps to find out if such massage can reproduce syncope.

Management

Acute or immediate management consists of;

• Stabilize the patient
• Hospitalize if necessary
• Intravenous fluids if necessary
• Give oxygen, glucose etc depending upon what caused syncope

Long tem (preventive) measures;

• Avoid precipitating factors
• Maintain good hydration
• Adequate food intake
• Avoid sleep deprivations
• Avoid excessive stress
• Leg exercises to improve blood return to the heart
• Tight leg stockings (especially for orthostatic hypotension)
• Medications (e.g. propranolol, fluoxetine, fludrocortisone, midodrine)

For carotid sinus syncope avoid wearing tight neck collar, ties etc, and also shaving precautions over the neck.

Patients prone for vasovagal syncope should avoid witnessing surgical procedures, blood drawing and other precipitating factors. Drugs like propranolol or fluoxetine are of some benefit.

Hypoglycemia, hypoxia, hyponatremia conditions are identified and treated.

Postural hypotension is treated with avoiding the culprit drugs if possible, postural adjustment, tight stockings etc. Medication like fludrocortisone or midodrine reduces postural drop in blood pressure and might be of some help.

Cardiac pathologies are identified and treated aggressively as there is a risk of death associated with this subtype of syncope.

Surgical options: If syncope is refractory to conservative management then for certain patients especially with vasodepressor type cardiac pacemaker is indicated. Cardiac defibrillator is a choice for patients with arrhythmias. Hybrid devices containing both the properties are available for suitable patients.

A stroke is an acute or rapidly occurring neurological manifestation caused by a reduction or absent blood supply to a particular region of brain, or caused by a bleeding. If stroke symptoms resolve completely within 24 hours then it is called as a TIA (transient ischemic attack).

Types of strokes

Mainly two types including;

• Ischemic
• Hemorrhagic

The ischemic stroke means the blood supply to the brain is blocked. In the hemorrhagic type the main culprit is the bleeding in to a discrete location in the brain and resulting brain dysfunction.

Ischemic strokes are of two types;

• Thrombotic
• Embolic

Thrombotic: In some people especially older and having chronic medical conditions like diabetes, high blood pressure, high cholesterol etc, a build up of cholesterol (a type of fat) along with blood cells called platelets take place along the inner margin of an artery and this is called as atherosclerosis. This can progress and gradually narrow the artery and when a critical build up occurs it can result in blockage of circulation causing damage to the organs supplied by that artery.

If that happens with the arteries supplying the brain then it results in ischemic stroke.

Embolic: Sometimes these atherosclerotic plaques built up inside the arteries may break up and the fragments may travel down the circulation and cause a blockage at a distal site once again causing stroke symptoms. These fragments are called as emboli (singular- embolus) and the phenomenon is called embolism. Such emboli may also arise from the heart chamber especially in the left atrium (left upper chamber) and enter the arterial circulation, reach the brain, cause blockage and stroke symptoms.

Blood circulation to brain

The brain is supplied by four major arteries; a pair of carotid and vertebral arteries (one on either side). Carotid arteries run up in the front aspect and the vertebral arteries on the back aspect of neck. The vertebral arteries unite to form basilar artery. All these arteries subsequently form an anastomosis called circle of willis. Various branches arising from the carotid, vertebral, basilar arteries as well as the circle of willis supply the whole brain.

Clinical manifestation (Symptoms)

What type of symptom is manifested depends upon the region of brain that is involved.

Cerebral hemisphere: Speech deficits (aphasia), paralysis of limbs, facial paralysis, decreased sensory perceptions etc.

Diencephalon (thalamus, hypothalamus etc): May produce decreased sensory perceptions etc.

Basal ganglia: May produce contra lateral limb tremors, muscle stiffness (rigidity), paucity or poverty of movements etc (so called parkinsonian features).

Brain stem: Limb paralysis and decreased sensation over the limbs with certain motor & sensory manifestation of the face, eyes, oral cavity, throat etc (involvement of cranial nerves) etc.

Cerebellum: in-coordination of limbs and truncal ataxia, gait unsteadiness etc.

In general the cerebral hemispheres are supplied by anterior circulation (carotid arteries) and the brain stem and cerebellum supplied by posterior circulation (vertebro-basilar arteries). Regions like basal ganglia, diencephalon are supplied by both anterior and posterior circulation with varying proportions.

Diagnosis

Stroke is a clinical diagnosis but to elaborate further on this basic diagnosis & to assist with the management the following tests are usually performed (as per the need);

• CT scan of brain
• MRI of brain
• Blood tests
• Carotid ultrasound
• Echocardiogram
• EKG/ Holter monitor
• Angiogram

If stroke has occurred in a younger patient (stroke in young, generally considered as age <45) then additional special blood tests need to be done.

If stroke is hemorrhagic and an identifiable cause is not detected like high blood pressure then additional investigations are necessary. In younger people if hemorrhagic stroke occurs then condition like AVM (arterio-venous malformation) are to be ruled out and the above two situations generally require a test by name angiogram.

Management

Acute management (general measures):

• Stabilizing the patient
• Hospital admission
• Control of blood pressure and other medical conditions

Specific measures:

• Medications to reduce brain swelling (mannitol)
• Clot buster treatment (lyses the clot, opens up the blockage)
• Intravenous heparin (blood thinner)
• Low molecular weight heparins (blood thinner)
• Anti-platelet agents (aspirin, clopidogrel etc; reduce thickening of arteries)
• Oral blood thinner (warfarin)
• Surgical measures (e.g. carotid endarterectomy)
• Physical, occupational, speech therapy as necessary.

If the symptoms onset is within three hours and no contraindication exists then clot buster treatment like tPA is given. This disintegrates the clot and re-establishes the circulation. There are pros & cons of this treatment and decisions to treat with it or not is made on individual case basis. Heparins (given as injections) are mainly helpful in embolic strokes and warfarin is the oral counterpart for the same purpose and usually taken on long term basis.

Please note that bleeding is a risk with all these above mentioned medications including clot busters, blood thinners& anti-platelet agents alike.

Chronic/ long term management (preventive measures);

• Anti-platelet therapy (aspirin, clopidogrel etc)
• Warfarin
• Control of blood pressure, diabetes, high cholesterol etc
• Physical, occupational, speech therapy as necessary.
• Healthy lifestyle (cessation of smoking etc)

Pseudo-tumor cerebri (PTC), now-a-days also called as idiopathic intracranial hypertension is a neurological condition characterized by abnormally raised pressure within the skull cavity and presents with severe headache & visual manifestations.

Inside the brain tissue there are cavity-like structures what we call as ventricles and the CSF (cerebrospinal fluid) flows through these ventricles. CSF is secreted inside the ventricles and it flows through them and exits the ventricular system and reaches the subarachnoid space, a CSF containing space formed between the two coverings of brain and spinal cord called as arachnoid & pia membranes. In PTC the CSF pressure is abnormally elevated and precipitates the above mentioned symptoms.

What Causes Pseudo-tumor Cerebri?

It is clearly known that the CSF pressure builds up in side the brain in PTC patients but as to  how exactly this abnormal raise in CSF pressure happens is still not clear although there are many hypotheses put forward. Impaired absorption of CSF is a dominant theory although it is difficult to explain if that is so then why not it results in hydrocephalus (enlargement of ventricles). All in all the genesis of PTC appears to be very complicated one.

By convention PTC is diagnosed only when it is idiopathic and no secondary causes are identified. Such secondary causes which can produce a similar picture include;

* Medications (e.g. tetracycline)
* Vitamin A and its derivatives
* Cerebral Venous thrombosis
* Endocrine disorders (e.g. hypothyroidism, OTC-oral contraceptive pills)
* Lupus etc.

Obesity is a common accompaniment especially of idiopathic PTC.

Clinical Manifestations

• Headache
• Blurring of vision
• Loss of vision
• Nausea
• Vomiting
• Double vision
• Swelling of optic nerve (nerve of vision) disc (seen while looking inside the eyes) etc.

Headache is generally diffuse and varies in intensity. The blurring of vision is a dreaded symptom as it indicates the optic nerve is getting involved due to the CSF pressure effect. If the disease progresses then there is threat of further damage to this nerve and loss of vision.

Diagnosis

The combination of characteristic symptoms along with swelling of optic nerve disc in a child-bearing aged woman with overweight or obesity is strongly suggestive of this condition. However these clinical findings themselves are not diagnostic and additional tests like mentioned below are necessary to confirm this condition;

• CT scan (CAT scan) of Brain
• MRI of brain
• CSF (cerebrospinal fluid) analysis

CT or MRI of brain is done first to look for any structural problems that might have caused a condition called hydrocephalus which also can mimic this condition. You look for large ventricles (hydrocephalus), tumors, other growths, cerebral venous thrombosis etc. Once all those have been ruled out the suspicion for PTC further strengthens. Sometimes you may see a relatively smaller than normal sized ventricles on CT or MRI and according to some experts it strengthens the possibility of PTC.

After structural problems are ruled out then a spinal tap (lumbar puncture) is performed. During this procedure a sterile needle is passed through your back in to CSF containing space around your spinal cord. First CSF pressure is checked and normally it is less than about 200 mm of water and anything above this value is suspicious for PTC.

The borderline values are sometimes difficult to interpret however if >250 mm water pressure is found it is more suspicious, and anything >300 in an appropriate clinical setting is nearly diagnostic of this condition. After the CSF pressure is recorded a relatively large volume of CSF is drained and some of this fluid is sent to lab. If lab report is normal then it is almost confirming this diagnosis. The large volume CSF drainage has therapeutic role as well.

Management

Depending upon the individual case the options include;

• Discontinue the possible culprits like OCP, Vitamin A, tetracycline etc
• Pain killers for headache
• Acetazolamide (Diamox)
• Furesemide (Lasix)
• Weight loss (strongly advocated)
• Serial spinal taps
• LP shunt
• VP shunt
• ONSF (Optic nerve sheath fenestration) etc.

Acetazolamide is thought to decrease CSF production and also has diuretic properties (excretes excess water through kidneys) and is commonly used for this condition. Weight loss along with this medication may be enough for mild to moderate cases. If acetazolamide doesn’t work or patients do not tolerate it then furesemide may be tried but it is not as effective as the other drug. Although electrolyte imbalance can occur with both it is more so with furesemide.

Serial spinal tap is generally advocated for moderate to severe cases however it is rarely practical and not frequently done in the recent times.

When the symptoms are not responding to the initial these measures then surgical options tried. LP (Lumbo-peritoneal) shunt is the placement of a catheter between the lumbar CSF space and peritoneum to drain the excess CSF. Another similar procedure is done where a catheter is placed in one of the lateral ventricles of brain and connected to the peritoneum to drain CSF. Although these procedures in general are effective the downsides are shunt failure due to displacement or blockage; and the risk of bleeding, infection, seizures etc.

ONSF or decompressing the optic nerve is performed when there is a threat of losing visual function. Please note that this procedure is done to preserve the visual function and it doesn’t relieve the other main symptom headache.

Poliomyelitis or Polio is a neurological disorder caused by a virus and results in paralysis of skeletal muscles and usually life long disability and rarely death.

What causes Polio?

This disease is caused by a virus by name poliovirus and there are three subtypes, type 1, 2 and 3. Type 1 is the most common. Polio virus affects only human beings.

How the disease results?

The virus gains entry to the body through the oral route after ingesting the virus through contaminated water or food arterial with feces of another infected person. It generally proliferates in the oro-pharynx and intestine. Majority of them do not suffer any problems at all. Some will develop symptoms of gastroenteritis including diarrhea etc. Only a small minority of people, approximately about 1 to 3% of those who harbor the virus in their GI (gastrointestinal) tract will go on to develop the neurological polio.

And the good news again is that those who develop neurological polio; majority of them will develop a condition called as viral meningitis (type of aseptic meningitis) and this is a self limiting illness. The unfortunate small minority of people will go on to develop what we call ‘paralytic polio’ and are of three types;

• Spinal polio
• Bulbar polio
• Bulbo-spinal polio

The polio virus invades the motor neurons of the spinal cord and brain stem (mainly medulla oblongata part) and induces severe paralysis of the muscles supplied by these neurons, and the resulting clinical manifestations are enumerated below.

Clinical Manifestations

Non-neurological polio;

• Asymptomatic
• Gastrointestinal polio: sore throat, fever, dry cough, diarrhea etc

Neurological polio;

• Aseptic meningitis: headache, fever, neck stiffness, malaise etc
• Spinal polio: asymmetric flaccid paralysis of limbs
• Bulbar polio: difficulty with swallowing, breathing, speech difficulties etc
• Bulbo-spinal: respiratory paralysis, difficulty with swallowing, flaccid limb paralysis etc

Diagnosis

Polio is generally diagnosed based on clinical features although for the confirmation of the diagnosis additional investigations are necessary including;

• Stool culture
• Throat culture
• Blood tests
• CSF (cerebrospinal fluid) analysis
• EMG/Nerve conduction study etc.

The stool & throat culture may help in isolating the virus. CSF analysis will assist in ruling out other infections of the nervous system and also sometimes confirming polio by isolating the virus. Antibodies to polio virus may be detected with blood tests. EMG (electromyography) and nerve conduction studies are certain special procedures which can pin point the pathology to the motor neurons and also rule out any other mimicking neurological conditions.

Management

• Stabilizing the patient
• Symptomatic treatment for fever, headache etc
• Hospitalization if necessary
• Breathing assistance if necessary
• Physical, occupational, speech therapy
• Preventive measures

There is no medication or antibiotic to kill the virus in the body means a cure for polio is not a possibility now, so patients are treated conservatively. Some patients especially the milder ones may recover completely. In majority of the survivors there may be at last some minor recovery is seen however many patients are left with major paralysis for life long. The above mentioned therapies are instituted at the earliest in the course of the illness to maximize the recovery of muscle function.

The preventive measures are of immense value when it comes to polio infection. There are very effective vaccines available. They are either in the injection or oral forms. Generally oral form is preferred because of the convenience of use. The vaccination program is a huge success and the incidence of polio has dramatically dwindled in most countries of the world. There is a reasonable hope that polio may be eradicable from the earth as smallpox. This is because for both the vaccines are highly effective also human beings are the only reservoirs for both these diseases.

Post polio syndrome

Post polio syndrome is a not an uncommon complication that occurs several years (usually few decades) after the previous polio attack. Patients will begin experiencing more weakness usually in the same affected limb however generally in the previously unaffected muscles. The exact cause is not clear however it is suspected to be due to over burdening and fatigue of the surviving nerve fibers that are supplying the muscles.

There are no diagnostic tests to confirm this condition however tests like EMG/NCS are helpful. MRI or CT of spine will help in ruling out conditions that mimic this syndrome.

There is no specific treatment for this condition so palliative therapy is what can be offered including non-fatigue exercise programs, using power-wheelchairs, analgesics if pain is present, reassurance etc.

Synopsis

• Polio is a highly disabling and rarely fatal viral disease.
• The facts that humans are the only reservoirs & availability of effective vaccination makes this disease amenable to eradication!

Idiopathic Parkinson disease (PD) is a progressive neurological disorder and is more commonly seen in older people. It begins with minor neurological dysfunction however during the advanced stages it usually has a crippling effect on its sufferers.

What causes PD?

There is a deficiency of a chemical substance called dopamine in the brain especially in a region called basal ganglia. This deficiency also results in the unrestrained activity of another chemical called acetyl choline. There is degeneration of the brain cells producing dopamine but as to what triggers this degeneration of brain cells is still not clear. Various hypotheses including environmental like exposure to toxins on a long term basis has been speculated.

Who gets it?

This disease occurs all over the world and incidence typically increases with age and majority of patients are >60 years. However younger people are not immune from this disease. Only about 5% of cases are hereditary. Rural living has been associated with some increased frequency of this disease.

Clinical Manifestations

Idiopathic PD produces certain very characteristic presentation and the four most typical symptoms include;

• Akinesia/ Bradykinesia
• Rigidity
• Tremors
• Postural imbalance

Akinesia / bradykinesia mean slowing of motor activities. A patient with PD will typically take longer time to finish a task which they used to finish faster before. For example patients take longer time to come out of the chair or bed. In fact almost all daily motor activities may slow down including chewing the food, swallowing, walking, turning, bending etc. As disease advances their eye blinking decreases, facial expressions diminish and give a mask like facial appearance.

Rigidity is a form of muscle stiffness and impairs their motor activities. Tremors are characteristically resting means when patients are not using the limbs they occur and as they initiate activities with the affected limb the tremor disappears or diminishes however usually return promptly when that limb is rested. Postural imbalance is a very troublesome symptom although it is not seen in the initial stages of PD.

PD symptoms typically begin on one side of the body then gradually spread to the other side and as disease progresses more and more disability accrues.

Diagnosis

Idiopathic PD is one of those neurological conditions that are essentially diagnosable only based on clinical criteria. So much so it is clinically diagnosable majority of the times you do not need any other investigations at all! No imaging studies of brain, no blood tests nothing needed with typical cases.

Investigation like a CT scan (CAT scan) or MRI of brain is necessary if the clinical presentation is atypical. Structural problems like tumors, stroke etc can mimic Parkinson disease to some extent and the above tests will sort it out.

Management

Once the diagnosis of idiopathic PD is made with certainty then you will grade the disease. This will assist the doctor as to whether to initiate treatment and if so what kind etc.

Generally the three sages of disease include;

• Mild or early
• Moderately advanced
• Late or severe

The treatment choices available include;

• Medications
• Surgeries
• Physical, occupational & speech therapies

In the early stages where the disease manifestations are mild & generally do not affect their life much, wait and watch is one of the best policies. Since the medications can produce side effects if you start them at this stage then you may be doing more harm than help. Patients are reassured and adequate exercise or physical therapy (PT) is advised to keep the patient fit, confident and flexible.

When disease is said to be moderately advanced frequently it starts bothering them in the personal, social & professional spheres. At this stage majority of the patients are on some medications. Exercise and PT continues as usual. A cane or walker is recommended to avoid falls.

In the late or advanced stage patients are severely handicapped. They need assistance for many or almost all of their daily activities. Their cognitive functions may be compromised too. The medications are continued as usual. You try to optimize the dose as long as side effects are minimal or tolerable. Surgical treatments are definitely contemplated at this level although not every patient might benefit from it.

Anti-Parkinson disease medications include;

• Levodopa
• Levodopa with carbidopa
• Bromocriptyne
• Selegeline
• Pramipexole
• Ropinirol
• Entacapone
• Tolnacapone
• Levodopa, carbidopa with Entacapone etc.

Levodopa is the most effective agent however after using it for few years its effectiveness diminishes; also certain uncomfortable side effects called dyskinesia & motor fluctuations may occur. So other agents like dopamine agonists (e.g. pramipexole) etc are tried first and levodopa is reserved for advanced stages.

Almost all above medications can produce varieties of side effects including;

• Dizziness (especially in standing position)
• Nausea
• Vomiting
• Diarrhea
• Visual hallucinations
• Drowsiness etc

Surgical treatments for PD include;

• Deep brain stimulation (DBS)
• Pallidotomy
• Thalamotomy etc.

Deep brain stimulation (DBS) has gained an enormous popularity in the recent times and the advantage with this procedure is no damage to the brain tissue is done and the electrodes can be pulled out later if wished so.

Also note that…

Although the advanced Parkinson Disease may severely restrict a patient’s physical abilities however the disease itself is not fatal. Generally patients succumb to this disease as they are prone to develop infections like aspiration pneumonias, urinary tract infections, sepsis etc. So an aggressive intervention to prevent such complications developing is of prime significance.

Geographical distribution

It seems there is certain environmental factor that is involved in the occurrence of MS; this strong notion is founded on the observation that this disease has a predilection for people living nearer to the poles of earth as compared to the equator region. Patients are in general seen all over the world but are clustered in the above regions.

What causes MS?

It is still a mystery as to what causes MS although the available evidences point towards a multi-factorial influence including environmental, viral infections, genetics etc. MS is not considered as a hereditary disease but genetics appear to play certain role.

What is the problem with MS?

MS is considered as a demyelinating disease as it damages myelin structure of brain & spinal cord. The brain cells (neurons) dispatch the neural signals through their long thread like structure called axons. These axons are wrapped up by a substance called myelin and it considerably enhances the speed with which neural signals are propagated from one place to another within the brain & spinal cord. If this myelin gets damaged the neural signals are not conducted properly from one place to another and this will clinically manifest with varieties of neurological episodes.

Clinical manifestations

MS affect the brain and spinal cord and not the other parts of nervous system. The 2nd cranial nerve (optic nerve, the nerve of vision) is considered as continuation of brain so it may get involved too. The clinical manifestation would depend upon what area of brain or spinal cord is involved. MS episodes characteristically are disseminated in time & space, what it means is episodes occur at different times and involve different areas of brain & spinal cord (of course this is not necessarily true for the progressive variants).

Frequent symptoms;

• Blurring or loss of vision in one eye (optic nerve)
• Numbness of limb/limbs
• Paralysis of limb/limbs
• Speech deficits
• Facial paralysis
• Gait unsteadiness
• Double vision
• Limb in-coordination
• Urinary bladder symptoms etc.

Types of MS

There are four types of MS;

• Relapsing & remitting (RRMS)
• Secondary progressive (SPMS)
• Primary progressive (PPMS)
• Progressive/Relapsing (PRMS)

The commonest type is the relapsing & remitting type and here patients experience recurrent neurological deficits however they gradually recover from them with almost no or only minimal residual deficits. Some of these RRMS patients later in the course of their illness develop a progressive course which is called as SPMS. In the primary progressive type there usually are no discrete neurological episodes rather it begins and progresses gradually until patients are severely handicapped. The PRMS patients’ begin with a PPMS course but later add on SPMS features.

Diagnosis

Other than brain-lesion biopsy no diagnostic tests are available for the confirmation of MS.  Even biopsy cannot be considered entirely diagnostic as there are other demyelinating conditions that can mimic MS.

MS diagnosis is accomplished using clinical & laboratory criteria. If all the criteria are met then it is Definite MS. If less criteria are fulfilled then we have either a probable MS or “at risk for MS’ categories.

The investigations necessary to arrive at the diagnosis of MS include;

• MRI of brain
• CT scan (CAT scan) of brain
• CSF (cerebrospinal fluid) analysis
• Evoked potentials etc.

MRI is certainly superior to CT for the detection MS plaques (lesions). CSF will show normal pressure, may be slightly increased cell count, elevated protein, normal glucose. A special test called oligoclonal band may be positive. Gamma globulins are generally elevated too. Myelin basic protein is another substance looked for in the CSF, although not specific but raises the MS possibility if found elevated.

Management

Immediate (acute) management

• Stabilizing the patient
• Hospitalization if necessary
• Intravenous steroid therapy
• Oral steroid therapy
• Physical, occupational, speech therapy as necessary

Long term care including preventive measures

• Disease modifying agents
• Symptomatic management
• Physical, occupation, speech therapy as necessary

The disease modifying agents include;

• Interferon beta 1 alpha
• Interferon beta 1 beta
• Glatiramer acetate
• Natalizumab (tysabri)
• Mitoxantrone (novantrone)
• Methotrexate
• Azathioprine
• Cyclophosphamide etc.

In general the preventive treatment begins with one of the first four agents mentioned in the above group. They are all in injection forms and depending upon the agent subcutaneous, intramuscular, intravenous etc. If these agents fail then the other agents mentioned in the above group are usually tried. They are anti-cancer therapies too (chemotherapy agents) and some of them given as injections only and others as injection or oral forms. The chemotherapy agents generally produce more side effects than the other agents mentioned above.

Synopsis

MS (multiple sclerosis) is a chronic neurological disorder with varied manifestations. Early diagnosis and institution of disease modifying agents is of paramount significance in minimizing the future attacks and long term disability.

Classification/Types of Brain Tumors

Brain tumors are generally classified as;

• Primary tumor OR
• Secondary tumor

Primary tumor indicates the tumor originated from the brain tissue or its coverings e.g. meningioma. Secondary tumor means the tumor originated somewhere else in the body and then reached brain by a process called metastasis e.g. lung cancer spreading to brain.

The primary brain tumors are further classified as;

• Benign tumors
• Malignant tumors (cancers)
• Benign or malignant

Tumors like lipoma are examples benign tumors & by and large they remain to be benign always.

Common brain cancers are;

• Glioblastoma multiforme (grade 4 astrocytoma)
• Anaplastic astrocytoma (grade 3 astrocytoma)
• Lymphoma
• Medulloblastoma (mostly in children) etc.

However many tumors of the brain can be either benign or malignant and examples include;

• Meingioma
• Astrocytoma (early stages)
• Ependymoma
• Oligodendroglioma
• Shwannoma
• Choroid plexus papilloma etc.

Brain tumors are also classified as;

• Intra-axial OR
• Extra-axial

Intra-axial tumor implies the tumor originated within the brain tissue e.g. astrocytoma, while extra-axial tumor means the tumor originated out side the brain and may spread in to the brain tissue e.g. meningioma.

Age plays some role too. Astrocytomas occur at any age, but when they occur in kids the favored location is brain stem and in adults, cerebral hemispheres. Certain tumors like medulloblastomas typically occur in children. Meningimoas are extremely rare in children. Pilocytic astrocytoma is more common in children.

Commonly encountered brain tumors

Some of the commonly encountered brain tumors include;

• Meningioma
• Glioblastoma multiforme (GBM)
• Malignant astrocytoma grade 3
• Malignant lymphoma
• Carcinmatous meningitis
• Medulloblastoma (children)

Meningiomas are generally benign tumors and arise from the meninges. They grow gradually and compress the neighbor brain tissue. GBM & malignant astrocytoma grade 3 are very malignant tumors and GBM is the commonest cancer of the brain. Malignant lymphoma is another aggressive tumor and arises generally in the setting of immuno suppression like AIDS. Carcinomatous meningitis occurs when tumors like lung or breast cancer spread to the meninges rather than to the brain tissue. Medlloblastoma is mostly encountered in children.

What causes Brain Tumors?

Tumors result due to excessive and abnormal proliferation of cells in a tissue. Normally there are inhibitory factors to keep a check on any such abnormal proliferation however due to one or other reasons when those curbing factors get dysfunctional unrestrained cell growth takes place and results in a tumor.

Clinical manifestations

This depends upon the location of tumor, generally you see;

• Local symptoms &
• Symptoms due to increased pressure in the skull cavity

Local symptoms occur due to the direct pressure effect of the growth on to the surrounding brain tissue. And as the tumor increases its size, the volume of the contents inside the skull cavity increases too, however the capacity of skull cavity being fixed it starts exerting pressure effect on the brain diffusely. This results in serious conditions like hydrocephalus (enlarged fluid filled cavities inside the brain called ventricles) and herniation of brain can take place too.

Common clinical manifestations with tumors are;

• Headache
• Vomiting
• Decreased level of consciousness
• Change in mental status
• Seizures
• Loss of consciousness
• Paralysis of limbs
• Sensory abnormalities
• Double vision etc.

Diagnosis

Once clinically a tumor is suspected your doctor will run several tests including;

• CT (CAT scan) of brain
• MRI of brain
• Biopsy
• CSF (cerebrospinal fluid) analysis etc

CT or MRI can show the tumor and to find out the exact type of tumor a biopsy may be needed where a small piece of tumor tissue is excised and checked under microscope.

CSF analysis is used for both diagnosis of a tumor (e.g. carcinomatous meningitis) or spread of a tumor, although sometimes spinal tap is contraindicated when brain tumor is present.

Prognosis

Brain tumors are heterogeneous which means the prognosis varies from tumor to tumor. In general cancerous growths fare the worst. For benign tumors like meingioma for most patients life expectancy is normal or only minimally reduced.

However please note that when it comes to brain tumors their cancerous nature alone doesn’t decide the outcome, for example whether they are operable, accessible to surgeon etc counts too. Somebody may be harboring a fully benign meningioma but in a surgically inaccessible area and the further growth of this tumor can be of catastrophical significance including death.

Management

• Stabilize the patient
• Hospitalization if necessary
• Steroids to reduce brain swelling
• Anticonvulsant medications if patient had convulsions
• Surgical excision of tumor whenever feasible
• Gamma knife surgery (a special type of radio-surgery)
• Chemotherapy
• Radiation therapy
• Physical, occupational, speech therapy as necessary

Synopsis

Early diagnosis and management are of paramount significance in dealing with brain tumors.

Migraine headache is a neurological condition characterized by recurrent episodes of severe headache and it is one of the commonest causes of headache. Women are affected more than men.

What causes Migraine?

The exact mechanism that triggers migraine headache is still unknown and various hypotheses including, neuro-chemical (serotonin, substance P), vascular & neural theories have been put forward.

Types of migraine

The different types of migraine include;

• Common migraine
• Classical migraine
• Complicated migraine
• Retinal migraine
• Basilar migraine etc.

For details please see below.

Clinical Manifestations

• Headache
• Prodromal symptoms
• Aura symptoms
• Nausea
• Vomiting
• Light bothering
• Sound bothering
• Dizziness
• Weakness/ malaise etc.

Migraine is characterized by severe and recurrent headache episodes usually lasting between 4 and 72 hours (3 days).  Prodromal symptoms occur in about 50% patient and include protean vague symptoms like mood changes, irritability etc. The aura is typically seen in classical migraine patients and it differs from the prodromal symptoms by its occurrence just before the headache & the experience of well defined symptoms like visual phenomena e.g. scintillating light patterns.

In common migraine the headache may occur on both sides and in a diffused manner but with classical migraine the headache is typically unilateral and throbbing in nature. Severity varies but generally on a scale of 1 to 10, majority of the sufferers’ claim 7 to 10. Nausea and vomiting are frequently seen. Patients claim light and sound bother them. Dizziness, weakness, malaise may accompany the headache too.

Complicated migraine presents with headache and a prominent neurological deficit like a stroke for example (paralysis of a limb).

Retinal migraine is characterized by headache and recurrent episodes of temporarily decreased vision or blindness in one eye.

Basilar migraine usually occurs in younger people especially young women and headache is accompanied with varieties of symptoms like speech difficulties, double vision, swallowing problems, dizziness, spinning sensation in the head etc.

Diagnosis

The migraine headache is mostly a clinical diagnosis, however there are certain structural problems of the brain that can mimic this headache and they include;

• AVM (arterio-venous malformations)
• Tumors
• Other growths
• Aneurysms/ bleedings
• Brain infections etc.

The commonly utilized investigations to detect these pathologies are;

• CT (CAT scan)
• MRI of brain
• Angiogram
• CSF (cerebrospinal fluid) analysis etc.

Management

Acute management;

• Stabilize the patient
• Hospitalization if required
• Medications for acute attacks

Chronic or preventive management;

• Medications to prevent migraine headache
• Lifestyle modification

During acute attacks if a choice exists patient should confine to a room that is noiseless and not bright. If nausea and vomiting occur they are treated with medications like domperidone, promethazine etc. And the medications which help with the acute migraine headache include;

• Triptan group
• Ergot group
• NSAIDs
• Narcotic pain killers
• Steroids
• Other agents

Triptan group of agents are highly effective and generally well tolerated. These agents should be taken at the onset of headache to be effective maximally. They thought to influence the activity of neuro-chemical serotonin favorably and abort the headache. There are many agents belonging to this group like;

• Sumatriptan
• Rizatriptan
• Naratriptan etc.

They all are available as tablets and some of them as injections & nasal sprays too. Although generally safe, they do rarely compromise blood flow to heart and brain and can precipitate strokes, hear attack etc. So they are either relatively or absolutely contraindicated in these patients as well as patients with high blood pressure.

The ergot chemicals like ergotamine are other commonly used anti-migraine agents. Ergot chemicals are usually combined with caffeine, which also possesses some anti-migraine properties and also to improve the patient’s alertness. Ergotamine Injection and nasal spray preparations are available too. In general the effectives of ergots are comparable with triptans although the side effect tendency is considered more. They can produce side effects similar to triptans as noted above also can compromise blood flow to fingers or toes and cause a damage called gangrene.

NSAIDs: These are the non steroidal anti-inflammatory agents that are used for varieties of pain conditions and common examples include;

• Aspirin,
• Ibuprofen
• Paracetamol
• Piroxicam
• Naproxen etc.

Some of them are available as injection forms too. In general they are not as effective as the triptan and ergot groups however they are useful alternatives to them and a combination of NSAID with above group of agents can have some additive effect.

Narcotic agents although effective are generally discouraged because of abuse potential. There are supposed to be used for excruciating headache episodes only when other agents fail and only on short term basis.

Status migrainosus is a severe form of migraine where intolerable headache continuous for several days. Hospitalization is generally necessary and a course of steroids may be tried in conjunction with other pain killers. Long term steroid usage is not recommended as they are notorious to create numerous health complications.

Preventive agents:

There are several effective preventive agents and they are recommended if a patient experiences frequent episodes. They reduce or eliminate the future episodes with regard to their intensity and duration however they are not curative, in the sense, if they are discontinued then headache might recur.

Common agents used are;

• Beta blockers (e.g. propraolol)
• Calcium channel blockers (e.g. verapamil)
• Anti-epileptic agents (e.g. sodium valproate) etc.

Lifestyle modification includes avoiding food stuff that might precipitate headache like monosodium gluconate, nitrates, tyramine, cheese, chocolate, ice creams etc; reducing stress as much as possible; avoiding smoking, alcohol and leading a healthy life style as much as possible.

Natural remedies like acupuncture, yoga, meditation etc may also be useful in some patients for relieving and avoiding migraine headaches.

Meningitis is a neurological condition associated with inflammation of meninges (the coverings of brain and spinal cord).

Meningitis is generally a serious and life threatening condition if not promptly treated. Early institution of antibiotics generally results in favorable out come however it is not a guarantee.

Please note that when the term meningitis is used it usually indicates brain meningitis. If meningeal inflammation occurs only around the spinal cord then it is preferably called as spinal meningitis, and when the process involves both brain & spinal cord then it is called as cranio-spinal meningitis.

What causes Meningitis?

The causes of meningitis include;

• Bacterial
• Viral
• TB
• Fungal
• Parasitic (e.g. amoebic)
• Chemical
• Drug induced etc.

Majority of meningitis is caused by microorganisms like bacteria, viruses, TB & fungi.

Bacterial meningitis:

The type of bacteria causing meningitis depends upon the age & immunity status of the patient.

New born & infants less than six months;

• Group B Streptococci
• Escherichia Coli
• Listeria monocytogens

Younger children;

• Meningococcal
• H influenza

Older children & adults;

• Meningococcal
• Pneumococcal

Elderly people & immuno-compromised;

• Listeria monocytogens
• Pneumoccoal
• Meningococcal
• H influenza

TB meningitis is produced by tuberculosis bacilli and incidence in very high in developing countries especially in children.

Fungal meningitis: Caused by fungi and Cryptococcus neoformans is the commonest cause. Immuno-compromised people are especially susceptible for this type of meningitis.

Viral meningitis: Caused by varieties of viruses and many of these viruses are frequently encountered by human beings in the form of respiratory tract infections, gastroenteritis etc.

Source: All these above mentioned microorganisms gain entry to the meninges through the blood or from contiguous structures like sinuses, nose, middle ear etc.

How does the patient present?

Common symptoms include;

• Fever
• Headache
• Vomiting
• Intolerant to light
• Intolerant to sounds
• Irritability, poor feeding in infants & young kids

Acute meningitis: The onset and evolution of the symptoms are rapid and usually just a few days e.g. bacterial meningitis.

Sub acute & chronic meningitis: Here the disease process builds up gradually over weeks to months e.g. TB meningitis.

On examination these findings may be seen;

• Neck stiffness
• Kerning’s sign (a clinical test for meningitis)
• Brudzinski’s sign (a clinical test for meningitis)
• Papilloedema (swelling of optic disc inside the eye)

In young children the neck stiffness may not be prominent.

Diagnosis

Investigations performed include;

• CSF (cerebrospinal fluid) analysis
• Head CT or MRI (generally done but not always needed)
• Various blood tests including cell count, electrolytes, blood culture etc
• Chest x-ray
• Urine analysis etc.

CSF analysis is the cornerstone around which the diagnosis and the treatment of meningitis lie. Typically you check the CSF opening pressure, Protein, glucose, cell count, bacterial antigens, gram stain etc. Additional test are done depending upon individual cases.

In bacterial meningitis you see elevated CSF opening pressure, protein, cell count and decreased glucose. The cells increased are mostly what we call neutrophils. Gram stain may show the bacteria. Bacterial antigens may be positive. Bacterial culture & sensitivity is also done for the proper identification of bacteria and choosing the correct antibiotics.

With TB meningitis the CSF findings may overlap with that of acute bacterial meningitis however the lymphocytes are usually elevated. CSF might grow TB bacilli. AFB stain may be positive. Bacterial tests including gram stain, culture & antigen tests should come normal.

Fungal meningitis produces CSF findings somewhat similar to TBM. CSF fungal stains, antigens, culture all may be positive. The TB CSF tests should come normal.

In viral meningitis CSF shows; pressure may be elevated, protein elevated, glucose normal, cell count elevated with increase in lymphocytes; gram stain, bacterial, TB, fungal panel are all normal.

Management

Bacterial meningitis: It is a medial emergency. Immediately after the spinal tap or sometimes even before doing it you will intiate an aggressive and combination antibiotic course by intravenous route. Once identification and cultural sensitivity of the bacteria is done you can use only specific antibiotics. A course of steroids is used too for the first few days. Additional agents like mannitol may be used to lower the brain swelling.

TB meningitis (TBM): Very grave form of meningitis with high death & complication rate. Aggressive anti-TB regime is used on long term basis with steroids for first few weeks.

Fungal meningitis: Usually seen in immuno-compromised patients like AIDS, patients on steroids etc. Cryptococcal meningitis is the commonest type of fungal meningitis. Prompt treatment with anti-fungal agents should be initiated at the earliest.

Viral meningitis: It is quite common but majority of them resolve without any complications or death. Patients are reassured, and treated symptomatically with pain killers for headache etc. HIV (human immuno deficiency virus, AIDS virus) too can cause meningitis. The prognosis depends on the underlying HIV infection rather the meningitis.

Chemical meningitis: Uncommon. It may occur when meninges are exposed to chemical agents like radio-contrast dye. Conservative management with a course of steroids is usually tried.

Drug induced: Uncommon. Usage of drugs like NSAID (non steroidal anti-inflammatory drugs like ibuprofen) can cause it. Promptly discontinuing the culprit drug is the best treatment along with conservative treatment.

Synopsis

• Meningitis (brain meningitis) is the inflammation of meninges around the brain.
• Many types of meningitis are serious & life threatening in nature.
• Early detection and institution of prompt treatment is of vital significance.