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Jul01
Current Trends in the Management of Epilepsy
Author: Dr Aaron de Souza
Type of Article: Invited Review
Published in: Souvenir of the Goa Conference of the Indian Medical Association (GIMACON), 2009


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Jul01
“Guillain-Barré Syndrome in Goa: A Prospective Analysis”
Author: Dr Aaron de Souza.
Category: Original Research, prospective descriptive study.
Journal: Archives of Goa Medical College, 2005.


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May25
Smells Like Parkinson’s Disease
Parkinson’s disease has always been primarily seen as a movement disorder resulting in symptoms of shaking, tremors, rigidity, and trouble walking. Interestingly, however, at least 90% of patients with Parkinson’s experience either loss or decreases in the sense of smell. Studies have shown that problems with olfaction actually generally precede the onset of other motor symptoms. Most people are not personally aware of changes in their olfactory acuity, but the increasing range and prevalence of smell tests offer a quick, easy, cheap, and non-invasive diagnostic test, as well as a measure of disease progression. In addition, the shift of focus for researchers from Parkinson’s as a motor disorder to a more global neurodegenerative disorder allows consideration of new paradigms about the causes and disease progression.
The cellular basis of olfactory dysfunction in Parkinson’s remains an enigma. Post-mortem studies have confirmed shrinkage of the olfactory bulb, but this fails to shed light onto the root causes as it only demonstrates the end effect. Experimental models of Parkinson’s have demonstrated various results such as protein aggregation in the olfactory bulb, changes in levels of neurotransmitters, microglial activation, and loss of cells in the olfactory bulb. However, as all of these effects are inter-related, none of these clarify the actual initial cause of damage.
Many of the hypotheses as to why olfactory dysfunction occurs and precedes other symptoms remain grounded in the long-held paradigm of Parkinson’s as a motor disease caused by the loss of dopaminergic neurons in the substantia nigra. For example, in some experimental models an increase in dopamine was found in the olfactory bulb. The researchers suggested this occurs as a compensatory mechanism in response to the loss of dopamine in the substantia nigra. As it has also been shown that sense of smell is particularly vulnerable to changes in dopamine, excess dopamine in the olfactory bulb would, thus, lead to olfactory dysfunction.
However, a number of other theories have been proposed suggesting that perhaps the olfactory bulb is the first brain structure to exhibit signs of damage because Parkinson’s could be caused by respiratory viruses or inhaled toxins that enter the brain through the nose. The cause of Parkinson’s has not been conclusively determined. And while a genetic component has been uncovered, the causes are clearly much more complex with various environmental factors involved. A number of studies have been performed demonstrating Parkinson’s-like symptoms following exposure to viruses, heavy metals, and pesticides in experimental models. Epidemiological studies have also linked pesticides exposure to an increased risk of Parkinson’s. It is certainly an interesting hypothesis that inhaled toxins could cross the blood brain barrier, and that the damage in Parkinson’s could begin first in the olfactory bulb and then spread from there to the substantia nigra. In addition, as the olfactory bulb is heavily involved in adult neurogenesis, any damage to this structure could severely limit the brain’s ability to repair itself by replenishing damaged neurons with new ones. Perhaps, then, Parkinson’s disease does not depend on a single source of damage, but rather multiple insults occurring. For example, genetically induced damage to the dopaminergic neurons in the substantia nigra combined with inhaled toxins damaging the olfactory bulb could, together, cause Parkinson’s, while one or the other would be insufficient.


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May23
Stem Cells: Myhts and Facts
"STEM CELL MYTH" ABOUT NEUROLOGICAL TREATMENTS: PLEASE STOP MISGUIDING PATIENTS

STEM CELL THERAPY IS NOT YET SCIENTIFICALLY PROVEN SAFE OR BENEFITIAL, NOR RECOMMENDED FOR ANY NEUROLOGICAL CONDITIONS. YET HUNDREDS OF PATIENTS ARE BEING TREATED WITH THIS FOR MULTIPLE SCLEROSIS, NEUROTRAUMA, PARKINSONS DISEASE ETC ETC.

ICMR SAYS:

9.3 Use of stem cells for therapeutic purposes 9.3.1 As of date, there is no approved indication for stem cell therapy as a part of routine medical practice, other than Bone Marrow Transplantation (BMT). Accordingly all stem cell therapy other than BMT (for accepted indications) shall be treated as experimental. It should be conducted only as clinical trial after approval of the IC-SCR/IEC and DCGI (for marketable products). All experimental trials shall be registered with the NAC-SCR.

http://icmr.nic.in/stem_cell_guidelines.pdf




Top 10 Stem Cell Treatment Facts | Closer Look

www.closerlookatstemcells.org

Many clinics that are offering stem cell treatments make claims about what stem cells can and cannot do that are not supported by our understanding of science. The information on this page corrects some of the misinformation that is being widely circulated.


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Mar03
STROKE TREATMENT
role of endovascular intervention in stroke treatment– By Dr. Sunil Bhargava
MD, DNB, MNAMS, STA certified equivalence CCST (UK)


Endovascular therapy is a well-established treatment modality for a variety of cerebrovascular central nervous system disorders. Neuroendovascular approaches provide treatment options for conditions previously thought to be untreatable. Ongoing device developments and refinements continue to revolutionize the field. These refinements, along with a better understanding of the disease process allow minimally invasive neuroendovascular techniques to be used for treatment acute ischemic stroke and stroke prevention.

The majority of ischemic strokes are due to thromboembolic arterial occlusion
75% occurring in the ICA distribution. While mortality from middle cerebral artery strokes is low, there is a high morbidity, with only 20 – 25% of patients returning to an independent lifestyle. Posterior circulation strokes are more ominous, with significant mortality rates, up to 86.4% in one study. Over the past few years, there has been intensive investigation of intravenous thrombolytic therapy for the treatment of acute ischemic stroke. At the present time, only tissue plasminogen activator (t-PA)/Urokinase, when administered within three hours of symptom onset, has definitively been shown to be an effective therapy.

The benefits of this therapy were demonstrated in the National Institutes of Neurologic Disorders and Stroke (NINDS) sponsored trial in 1995.This trial led to the FDA approval of t-PA for stroke treatment in June 1996. At present, only a small fraction of potentially eligible stroke patients are receiving treatment. The primary reason that patients are not eligible for this treatment is the very short, three-hour time window from symptom onset in which the agent should be administered. Intra-arterial recombinant t-PA (rt-PA) is suggested to be more effective than intravenous rt-PA. In local intraarterial (IA) thrombolysis, fibrinolytic agents are infused distal to, proximal to, and directly within thrombotic occlusions of main stem cerebral arteries, using an endovascular micro catheter delivery system. The dosage used is 0.3 mg/kg, up to a maximum of 10-20 mg intra-arterially. Direct infusion of thrombolytic agent near the thrombus allows greater concentration of agent, fewer systemic effects, more rapid dissolution of large
or multiple clots and an opportunity to carry out gentle mechanical disruption of the clot with the delivery catheter and wire. IA thrombolysis also has a number of potential disadvantages, including manipulation of a catheter within cerebral vessels, potentially increasing vulnerability to hemorrhage; the requirements for systemic heparinization during catheterization to deter catheter-induced thrombosis; and delay in initiation of thrombolysis.
The procedure is labour and capital intensive, and the number of facilities skilled in IA thrombolysis is small. Intra-arterial thrombolysis may be used in the anterior circulation (carotid circulation) up to 6 hours after onset of symptoms, although better results have been shown when administered within 3 hours. It is also used up to 12 – 24 hours after onset in posterior (vertebrobasilar) circulation lesions, because of the poor prognosis without therapy.

Despite the increased rate of symptomatic hemorrhage with intra-arterial administration of rt-PA, many trials have still demonstrated improved clinical outcomes versus placebo Of particular note is the first Phase III trial of IA thrombolysis, the Prolyse in Acute Cerebral Thromboembolism II (PROACT II) trial (5). In PROACT II, patients within 6 hours of symptom onset with symptomatic M1 or M2 middle cerebral artery (MCA) occlusions were randomized to receive IA thrombolysis with systemic heparinization vs. heparinization alone. The prespecified primary outcome in PROACT II, a good or excellent score on the modified Rankin Scale of handicap, was achieved by 40% of the IA group vs. 25% of control patients (p=0.043). In addition, recanalisation rates 2 hours after initiation of infusion were markedly increased in the IA group. Intracerebral hemorrhage rates at 36 hours were increased in the IA group; however, no difference in overall mortality between the two groups was observed.
Another potential role for intra-arterial rt-PA is for postoperative stroke patients. The risk of stroke is approximately 2.9% in the immediate postoperative period. During a recent multicenter study of intra-arterial rt-PA administered during the immediate postoperative period, good results were obtained with only minimal complications. The local delivery of thrombolytic agent reduces systemic effects. Only patients who had previously undergone intracranial surgery had an unacceptably high complication rate. Further research is being conducted in the use of mechanical thrombolytic devices, as well as laser clot fragmentation. The advantages of these approaches include lack of systemic and hemorrhagic complications. Better public awareness is also needed, since fewer than 5% of eligible stroke patients actually receive thrombolytic therapy. In addition, faster diagnosis with MR diffusion and CT perfusion may help to identify patients who can benefit from thrombolysis.
Carotid artery stenting has important role in preventing stroke. It is of particularly suitable in case unfit for surgery, unfavorable anatomy, tandem lesions and relatively poor medical risk.


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Feb06
Facial palsy
Facial palsy is condition in which there is lesion of the facial nerve and the resultant paralysis in the muscles that it supplies. So there will be following features on the side of lesion:

Loss of facial expression.
Drooping of the face- Low eyelid, eyebrow and corner of mouth sag.
Closing the eye is difficult.
Eating is difficult because food collects in the side of the cheek and fluid seeps out of the corner of mouth.
Speaking, whistling and drinking are impaired.
Non-verbal communication is lost as the patient cannot register the pleasure, laughter, surprise, interest and worry.
The patient tends to sit with the hand over the side of face.
*
There is difference between an upper motor neuron lesion and lower motor neuron lesion of the facial palsy.

A unilateral UMN lesion usually spares the forehead as it is also innervated from the other side of the brain (part of facial nucleus supplying the upper face principally the frontalis muscle receive the supranuclear fibers from each hemisphere); however an LMN lesion affects all of one side of the face.

An upper motor neuron lesion causes weakness of lower part only of face on the side opposite the lesion. The frontalis muscle is spared; the normal furrowing of the brow is preserved, and the eye closure and blinking are not affected. The earliest sign is simply slowing of one side of the face, for example on baring the teeth or smiling.
Moreover, in upper motor neuron lesion there relative preservation of spontaneous 'emotional' movement (e.g. smiling) compared with voluntary movement.

A unilateral lower motor neuron lesion causes weakness of all the muscles of facial expression on the same side. The face, especially the angle of the mouth, falls, and dribbling occurs from the corner of the mouth. There is weakness of the frontalis and of eye closure since the upper facial muscles are weak. Corneal exposure and ulceration occurs if the eye does not close during sleep. The platysma muscle is also weak.

Causes of facial weakness:

These are as under:
The common cause of facial weakness is a supranuclear lesion (UMN) e.g. cerebral infarction leading to upper motor neuron facial weakness and hemiparesis.
Lesions at four other levels may be recognized by the associated signs.

PONS. The sixth nerve (abducens) nucleus is encircled by the seventh nerve fibers and is therefore involved in the pontine lesions of the nerve, causing lateral rectus palsy.
If there is accompanying damage to the neighboring centre for the lateral gaze (PPRF) and the cortispinal tract, there is the triple combination of:

LMN facial weakness
Failure of conjugate lateral gaze (towards the lesion)
Contra lateral hemi paresis

Causes include pontine tumors (e.g. glioma), demyelination and vascular lesions.
The facial nucleus is affected unilaterally or bilaterally in poliomyelitis and motor neuron disease; the lateral usually causes the bilateral weakness.

CEREBELLOPONTINE ANGLE. The fifth, sixth and eight nerves are affected with the seventh nerve in lesions in the cerebellopontine angle where they are grouped together. Causes are acoustic neuroma, miningoma and secondary neoplasm.

WITHIN THE PETROUS TEMPORAL BONE. The geniculate ganglion (a sensory ganglion for taste) lies at the genu of the facial nerve. Fibers join the facial nerve in the chorda tympani and carry taste from the anterior two third of the tongue. The (motor) nerve to the stapedius muscle leaves the facial nerve distal to the genu.
Lesions of facial nerve within the petrous temporal bone cause:
Loss of taste on the anterior two third of the tongue
Hyperacusis (an unpleasant loud distortion of noise) due to the paralysis of the stapedius muscle
Causes include:
Bell's palsy
Trauma
Infection of middle ear
Herpes zoster (Ramsay hunt syndrome)
Tumors (e.g. glomus tumor)

WITHIN THE FACE. Branches of the facial nerve pierce the parotid gland and supply the muscle of the facial expression. The nerve can be damaged here by parotid gland tumors, mumps (epidemic parotitis), sarcoidosis and trauma. The nerve is also affected in the polyneuritis (e.g. G.B. Syndrome) usually bilaterally.
Weakness of facial muscles also occurs in primary muscle disease and disease of neuromuscular junction. Weakness is usually bilateral. Causes include:
Dystrophia myotonica
Facio-scapulo humeral dystrophy
Myasthenia gravis

Bell's palsy
This is a common acute, isolated facial nerve palsy believed to be due to viral infection (most probably herpes simplex) that causes swelling of the nerve within the petrous temporal bone.

MANAGEMENT:
Spontaneous recovery occurs toward the end of second week. Thereafter, continuing recovery occur. Fifty percent recover within three months. Continuing recovery may take 12 months to become complete. About 15 percent of patients are left with a severe unsightly residual weakness.

Medical:

Steroids (prednisolone 60mg daily reducing to nil over 10 days.)
Acyclovir for viral infection

If there is severe residual paralysis, cosmetic surgery and/or reinnervation (nerve anastomosis of the lingual to the facial) are some times performed after a year has been elapsed.

Physiotherapy:

During the paralysis:

The selection of the suitable physical agent depends upon the experience or the choice of an experienced physiotherapist. Physiotherapist may choose from a number of physical agents available.

Ultrasound is given over the nerve trunk in front of the tragus of ear and in area between mastoid process and mandible. There is no fear of applying ultrasound while doing the treatment of patient with Bell's palsy. The ultrasound is always applied on the side of lesion in front of the tragus of ear & in area between the mastoid process and mandible where the maximum tenderness of the facial nerve is determined by palpation. It is applied in slow circular motion with a starting dosage of 1 watt per square centimeter for 10 minutes. The dosage may be increased on the subsequent sessions if no remarkable improvement is noted. Let me explain that ultrasound waves cannot traverse the bone. That means ultrasound has zero penetration in the bone. Infact, ultrasound waves are reflected away from the bone. So there is no fear in applying the ultrasound on face. (This is only for LMN lesion type)

Low level laser therapy (infrared 808 nanometer wavelength 400 mill watt power for 5 minutes continuous)

Infra-red: Infra red may be applied to warm the muscles and improve the function, but you must ensure that eyes are protected with linens when you are applying infra-red to face. Timing should be for 10 to 20 minutes at a distance usually between 50 and 75 cm.

Ultraviolet Therapy: Formerly ultraviolet was frequently used to give third or fourth degree erythema doses over the facial nerve trunk and in area between mastoid process and mandible (at the point of emergence of facial nerve on face)to combat the infection and inflammation. The type of lamp used for this type of treatment is the Kromayer lamp. The Kromayer lamp is a water cooled mercury vapor lamp which eliminates the danger of infrared burn. It has the advantage that it can be used in contact with the tissue or with suitable applicator it can be used to irradiate a suitable body cavity.

Testing the dosage can be done with Kromayer lamp in contact with the skin, so very small holes are used, e.g. 0.25 square cm. since exposure time need only be very short. It is often useful if the Kromayer lamp has standard dosage time recorded on it for contact and 10 cm. The front of the Kromayer lamp is cleaned with an appropriate solution and when it has had its full 5 minute warming up period the lamp is ready for use. The front of the lamp is held as close as possible to the skin or the target tissue. At least an E4 dosage is given. Treatment could infact be given at a set distance of, say 4 cm.

Microwave diathermy: As far as micro wave diathermy application is concerned, there is strict contra indication for the use of micro wave diathermy for the treatment of face as micro waves can spread randomly and can damage the lens of eye causing the opacity of the lens. So there is no room for the application of micro wave to face.

Short Wave Diathermy: SWD can be safely applied for the treatment of facial palsy at the point of emergence of nerve on the face. The technique used may be monopolar or bi polar. In bipolar technique using the capacitor field method or induction or cable method, the one facial mask electrode is used as an active electrode for applying the rays to face while the second or indifferent electrode used on some distant part of the body (usually cervical or dorsal spinal area) to complete the circuit. In monopolar electrode method only one electrode is used to direct the rays to the target treatment area site and no second electrode is used at all. The treatment time is between 10 and 30 minutes. Shorter sessions are used for mild conditions. Treatment is given on daily basis to produce the required results.

Electrical Stimulation: The only form of electrical current used on face is interrupted direct current (I.D.C.) whether or not there is reaction of degeneration. This is requested only to preserve the bulk of facial muscles and to prevent their atrophy while waiting them to be in function whenever their re innervations arrives in case of axotomesis or reconduction after neurapraxia if the nerve is not damaged completely. There is no room for the use of faradic current use on the face as it could lead to cause secondary contractures of the face. Moreover, most patients find it intolerable on face due to its unnecessary uncomfortable sensory stimulation. The is due to the reason that the faradic current has a frequency of 50 cycles per second, and so produces the tetanic contraction of the muscles that it stimulates. Although for muscle contraction faradic current is surged to produce alternate contraction and relaxation yet the tetanic type of contraction produced by these 50 pulses delivered in just one second, is not required on face. The face muscles are very thin and delicate and could not tolerate this tetanic type of contraction and may be damaged to produce the secondary contractures. If secondary contractures are produced, all form of electrical stimulation should be abandoned temporarily to avoid further damage to the muscles. The face should be gently stretched and massaged.

Heliotherapy: I have found traditional old lay men to use the convex*lens to focus the sun rays to produce the third or four degree erythema dosages to facial nerve trunk and in area between mandible and mastoid process behind the ear and it frequently give dramatic result with excellent recovery of facial palsy.* The treatment was needed to repeat after one week to repeat the same session of the dosage.* Only three or four sessions of this kind were needed to*do the excellent management of the patient.* Infact, it is one kind of heliotherapy treatment which is available from the natural source of power i.e. the sun.** This is*most common form of physiotherapy medicine that is used by*conventional lay men here in Pakistan with excellent results of the treatment.* Please, note that sun rays are a mixture of infra red rays and ultraviolet rays and visible rays on the electromagnetic spectrum. The thermal effect is produced by the infra red portion of the sun rays while the chemical effect like tanning of skin, effect on photographic film, formation of vita. D is due ultraviolet portion in the sun rays. The visible rays which are near to infra red portion on the electromagnetic spectrum produces effects similar to infra red rays. The visible rays which are near to ultra violet portion on an electromagnetic spectrum produces effects similar to ultraviolet rays. The erythema formation is due to ultraviolet portion of the sun rays. Usually fourth degree erythema dosage is required to produce the required therapeutic results.

Iontophoresis: Zinc, potassium iodide or chloride iontophoresis is given to the affected ear to treat the otitis media if there is infection of the middle ear.

Massage: The patient derives great benefit from the massage. Massage may be taught to the patient.
Stroking in the upward, outward direction. It is given from chin upwards to the temple and from the middle of forehead downwards towards the ear. The technique should be gentle but at the same time stimulating.
Slow finger kneading applied over the paralyzed muscles maintains skin suppleness and muscle elasticity. Small circular finger kneading can be given all over the affected side of the face, care being taken not to stretch the muscles.
Tapotement may be administered in the form of tapping quickly and lightly with the finger tips. It must be done very gently over the forehead and superficial ridges, where only a thin layer of muscle covers the bone.
Frictions are given at the point where the nerve enters the face to soften any inflammatory deposit.
Vibrations performed with the tip of one or two fingers can also be used over nerve trunk at this point or they may be administered by placing the whole flat hand on the affected side of face.
These techniques applied daily for 5 minutes or so help to maintain lymphatic and blood flow and prevent contractures.

During Recovery:

PNF techniques are used for re-education:
Quick stretch can be applied to regain raising of eye brow and the movement of the corner of mouth.
The physiotherapist can produce the movement passively and then ask the patient to hold, and then try to produce the movement.
Icing, brushing, tapping or brisk stroking may be applied along the length of the muscles. e.g. Zygomaticus
Exercises:
Look surprised then frown
Squeeze eyes closed then open wide
Smile, grin, and say 'o'.
Say a, e, i, o, u.
Hold straw in mouth-suck and blow
Whistle

Please, add more suggestions and your own point of view regarding the treatment of facial palsy, mail us - info@bprc.in or visit www.bprc.in


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Feb06
The Prehospital Stroke Scale
Do a quick prehospital assessment when in doubt of a stroke event and save a life. Time is brain.
1.) Facial Droop ( have pt show teeth or smile)
-Normal: both sides of face move equally.
-Abnormal: One side of face does not move as well as the other side.
2.) Arm Drift ( pt closes eyes and extends both arms straight out, with palm up for 10 seconds.
- Normal: both arms move the same or both arms do not move at all ( other findings, such as pronator drift may be helpful)
-Abnormal: one arm does not move or one arm drifts down compared to the other.
3.) Abnormal Speech: ( have the patient say " you cant teach an old dog new tricks" ) may use pts primary language( if pt doesnt speak english) using any complete sentence.
Normal: pt uses correct words with no slurring.
Abnormal: pt slurs word, uses the wrong words or is unable to speak.
Interpretation: According to AHA guidelines, if any one of these three signs is abnormal, the probability of a stroke is 72%


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Nov14
Brain attack- stroke
Please visit my website www.irtreatments.com for detailed information.
Stroke-Brain attack- treatment and prevention
1.Acute stroke treatement
Stroke is a medical emergency which needs to be treated early and urgently to minimize the damage caused by such event. Very year large number of patients in city of Mumbai suffers from disabling stroke resulting in death and disability with huge cost to the families emotionally and financially.
In stroke “time is brain”, earlier the treatment, better the outcome. You should reach appropriate centre/hospital at the earliest.
2.Stroke prevention
• Life style- Eating a balanced diet is important.
• Medication- Your doctor will determine which medicines may be best for you.
• Angioplasty- The two carotid arteries are the main arteries carrying blood to the brain. They can become narrowed (more than 70%) in the neck by a buildup of cholesterol and other fatty material. You may be benefitted by angioplasty .


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Nov14
Brain aneurysm Treatment-Endovascular Coiling of Aneurysm
Please visit my website www.irtreatments.com for detailed information.Brain aneurysm Treatment-Endovascular Coiling of Aneurysm
Disease-Brain Aneurysm, Treatment-Endovascular Coiling of Aneurysm
Brain aneurysm is a disorder in which a bleb is formed in the brain arteries. When it leaks or ruptures it leads to catastrophe. This bleb or out pouching can be treated by angiography methods. One reaches the out pouching by a catheter and places coils with in it, till it gets blocked.


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Jul03
Bell's palsy
Facial paralysis rt or lt side


Bell 1 M / BD


SANG CAN 30 / QID
X 3 DAYS RT SIDE
SPIGELIA 200 / QID
X6 DAYS LT SIDE


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