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    Grumpy Old Man- My consultant

    "Doctor, this patient wants to be seen by you". I was in the middle of clinic when the nurse barged in & dumped a giant set of notes on my desk. "Mrs Cook does not want to see the consultant". My consultant, nicknamed "Grumps", short for "Grumpy Old Man". He is not the most friendly of characters, to put it diplomatically.

    When I saw Mrs Cooks said, "I don't want to be seen by the consultant, because the last time I saw him, he hardly spoke to me". Mrs Cooks fumed, "He never asked me what I wanted & didn't listen when I told him I did not want to be investigated any further. I was examined & sent for 5 different tests including X-Rays, ultrasounds, blood tests & ECGs. I was here nearly 5 hours last time."

    I was not surprised by what I was hearing. I have seen how Grumps interacts with his patients. They are made to sit in the corner in silence whilst he pours through the notes. The atmosphere would be similar to a naughty pupil sitting in the headmaster's office. After a long deafening silence, he would instruct the patient to undress for examination. Without further explanation, the patient would then be sent on his or her way for an exhaustive battery of tests taking up to several hours. 

    After all the results are back, the patient would then be summoned back to Grump's room where he would pronounce his verdict & treatment plan. If the patient dared to as so much question him, he would give them a patronising look, simply repeat his verdict & treament plan without elaborating any further. At the end of the consultation, the patient would be dismissed with the phrase, "that will be all".

    Its absolutely embarassing to watch this display. I can't believe how little he communicates to the patient. Until then, I didn't realise that doctors like this existed anywhere except on television as caricatures.

    Grumps unfortunately, is a relic from a bygone era where patients were talked at, not talked to. He is an excellent, knowledgable clinician & even has many patients that adore him. But his clinical practice fails on the communication skills side. He gives doctors a bad name & lets patients down. Even to his fellow doctors, Grumps remains a poor communicator, in particular those junior to him. He is capable of communicating well with fellow consultants, so its because of a lack of will rather than a lack of ability. Grumps has been working in the same hospital for over 30 years. He is head of department & has many powerful allies.

    It will not be easy to change him. Suggestions anyone?

    Dolichocephaly: An Info-graphic Article

    Dolichocephaly, also know as Scaphocephaly is a developmental ‘abnormality’ of the skull shape and size. Scaphocephaly itself means boat shaped head. Babies with dolichocephaly are born with a elongated head than a normal child. The anierior posterior diameter (length) of dolichocephaly head is more than transverse diameter (width). It has a incidence of 1 in every 4200 babies.
    Babies with dolichocehaly are not abnormal. But dolichocephaly may be associated with other underlying congenital abnormalities.
    Diagnosis of Dolichocephaly
    Dolichocehaly is detected as an increased cephalic index of less than or equal to 75. Cephalic index is calculated using two fetal bio metric parameters which are the occipitofrontal diameter  and the bipareital diameter. It is calculated as:
      cephalic index (CI) = bipareital diameter (BPD)/occipitofrontal diameter (OFD) x 100
    It can be diagnosed incidentally with USG, feotal skull X-ray or CT scan.
    Cause of Dolichocephaly: 
    Dolicocephaly may be just a normal variation to a sign of underlying developmental, genetic disorder.
    Premature closure of Sagittal suture lines Dolichocephaly is more common in breeech presentation Associated with long standing Oligohydramnios
    Association with other diseases, syndromes :-
    Marfan Syndrome Sotos Syndrome Crouzon Syndrome Sensenbrenner Syndrome Proteus Syndrome Bloom Syndrome Yunis-Varon Syndrome Deletion of 10q Do dolichocehaly always need treatment?
    Only symptomatic cases or cases with probable brain development issues require intervention. Rest actually do not need anything. The odd shape of the head can be compensated with hair styling easily in a grown up kid.
    Resources: NCBI, Radiopedia, 
    Related Reading : Cushing’s Triad, Paracetamol Overdose, Sgarbossa Criteria, Acne Vulguris, Coarse Ventricular Fibrillation, SiGECAPS


    SIGECAPS or SIG-E-CAPS is a popular mnemonic used to describe the eight signs of major depressive disorder (MDD). Major depressive disorder is also known as major depression, unipolar depression or clinical depression. It’s persistent low mood and self esteem or such episodes of two or more weeks, without a history of Manic, Mixed, or Hypomanic Episodes. When these episodes are accompanied, it’s a bipolar disorder and not MDD. The depressions in MDD doesn’t arise as a result of other psychosis, substance abuse, trauma or other medical conditions.

    SIGECAPS are the 8 below signs of Moderate depressive disorder. To diagnose MDD  at least 5 signs of SIGECAPS must be present for at least two weeks of duration.
                Sleep disturbance – Sleep disturbance may be in the form for increased or decreased sleep. Early morning wake up, late night sleeplessness, oversleeping, laziness or any of these may be associated.             Interest reduced – Lack of interest leads to zero initiative and drive. Day to day life both at work and home suffers. Individual tends to pend anything and everything. Also sex drive is reduced.           Guilt sensation and worthlessness – This happens without any reason. Patient starts thinking that, whatever he did was all wrong and he has no personal value in the society. He starts avoiding contact with people and social atmosphere.            Energy loss and fatigue – Lack of energy is obvious and goes side by side with reduced interest. Easy fatigability without any physical disability is another sign.           Concentration problems – Fleeing of Ideas, lost look, disinterested attitude leads to loss of concentration. This causes memory issues and frequent forgetfulness.           Appetite – Appetite may be increased or decreased markedly.           Psychomotor – Psychomotor agitation or retardation may show up.  It involves a aggravated or slowing-down of thoughts and change of physical movements in an individual. Psychomotor retardation can cause a visible slowing of physical and emotional reactions, speech and affect.           Suicidal tendency or Suicidity  –  At severe stages, frequently a MDD patient may have suicidal thoughts.  In the United States, around 3.4% of people with major depression commit suicide and up to 60% of people who commit suicide had depression or another mood disorder. So, SIGECAPS is just Sleep ,Interest, Guilt, Energy, Concentration, Appetite, Psychomotor and Suicidity
    Related Reading : Dolichocephaly, Paracetamol Overdose, Sgarbossa Criteria, Acne Vulguris, Coarse Ventricular Fibrillation, Cushing’s Triad,

    Can Hepatitis C Transmit In Modern OT?

    A few days back, a 28 years old married lady reached to emergency. She is mother of two, looks very ill, emaciated and restless. On enquiry, she gave history of pain abdomen for last one week. Pain was colicky and intolerable since last two days. Located to left lower abdomen. Her old documents showed ongoing treatment for PID. She does also have 9 mm left renal calculus and positive h/o HCV. After a dose of injectable antispasmodic, she was relieved and fell asleep. Some times later, her husband reached me alone, and started weeping. He told that she was operated in a hospital (name kept hidden) for laparscopic cholecystectomy 5 months back. Until then, she was perfectly fine. But following surgery she never recovered and 2 months after was diagnosed as HCV positive. She doesn’t had blood transfusion. Of course she had undergone various lab tests before that.  I assured him, that it’s not possible of HCV transmission in an OT. But in the back of mind, I, myself was not satisfied. After a few days while going through a few articles in the CDC website I discovered something else. The extract is as follows :-
    Source: Centers for Disease control and Prevention
    Now, as we don’t have as organized health investigative system, it’s hardly be possible to trace down the source. But it’s an eye opener to me.

    What is Substance Abuse

    What is Substance Abuse

    Substance abuse indicates something is being used to produce intoxicated effects in the body. It’s commonly due to addiction for ‘kick’,  taste or may be psychological demands. Substance abuse is synonymous with drug abuse, which is one of it’s kind. This article will give readers a glimpse on what is substance abuse, substance abuse drugs, causes, treatment options, and  prevention.

    What are used for Substance abuse

    Before reading further what is substance abuse, one must know the substances. Most commonly and widely used substances are alcohol, tobacco in different forms, cocaine, heroin, cannabis, opioids, amphetamines, barbiturates, benzodiazepines and methaqualones. There may be many other chemicals or drugs that are being used for such purposes, but not listed in substance abuse.

    Why people become victim of substance abuse

    The exact cause of substance abuse is not clear. It usually starts as occasional, out of fun, for stress relief or as performance enhancer. Gradually the body hunger or mind hunger is developed for that drug. Finally it overpowers judgement and he or she can’t help but to consume it more and more. The physical theory alone can’t explain substance abuse. That’s why substance abuse is termed as a social problem. Following factors are likely to influence development of substance abuse in a person

    Genetic predisposition

    Not an established theory. But there may be some genetic correlation where some people do develop addiction or urge to abuse drugs easily than others.

    From friends and families

    Exposure to drugs and learning to abuse with such materials from friends is the commonest cause. A boy may become victim of drug abuse, well before he understands how harmful it is. A family in which substance abuse is common among other members, children would likely to follow the same path.

    Social Issues

    Orphans, single parent, children of divorcees, single child, working parents, battered baby are more prone to develop such abuse. This is mainly due to lack of adequate social care, attention and depression. A child born and brought up in an ideal community, with company of good neighbors, friends and families are less vulnerable. Education, book reading, morality, truthfulness, teaching on right and wrong does have a great impact on character building of a growing child. In today’s life style,  parents spend less time with their kids, making them attracted to materials, internet, video games  etc. This is an earliest negative social behavior that seen commonly.

    Self Control

    Some people, though may consume such substance, they never become addicted. People may not even come to know that they used to consume. It’s not same with all. Gradually many of them become frequent abuser and finally become addicted.

                  Substance abuse is very common in today’s society. Most of the teenagers today become the victim of substance abuse between 14-16 years of age. So, what’s the early signs of substance abuse? This topic will elaborate the most likely signs of substance abuse in all ages.

    X-Ray and Pregnancy

    X-rays and Pregnancy related issues are worth discussing here. Due to ignorance and accidental exposure to x-ray happens.  People frequently ask and seek advice on safety of security equipment,  metal detectors, airport security systems and scanners. Sometimes doctors  advise x-ray or CT scan in pregnancy, but never as routine. There are  misconceptions on X-rays and pregnancy. Lets  discuss the facts:
    How You May Get Exposed to Radiations:
    1.    Most of the accidental exposure happens when you go for X-ray not knowing that you’re pregnant. A woman conceives before she misses her first period.  Similarly health workers get exposed, but accidentally.  Risk of exposure in health workers higher than you.
    2.    Many a times, doctors may suggest an x-ray or CT scan. This may be to diagnose some fetal abnormalities (e.g., Heart Disease)  or due to other unavoidable situations. In this case, the CT scan is considered more important than the risk involved.
    3.    Today’s airports are equipped with  full body x-ray scanners. This is another form of exposure and very common form of exposure.
    4.    Rarely, a pregnant woman may get exposed to very high dose of radiation from malfunctioned equipment, accidents and disasters in factories ( occupational exposure). This is dangerous and may harm the baby.
    Facts on X-ray and Pregnancy
    1.    It is highly recommended to avoid x-ray exposures during first trimester ( First 3 months of pregnancy)
    2.    Single exposures or exposures before knowing that you were pregnant, the baby should be unharmed. X-rays harm the most when it’s repeated several times or in very high doses.
    3.    Even X-rays or CT scan done on you or your baby in the womb, do not harm your baby when advised by your doctor.  Your doctor suggests you the best timing and all safety precautions for such investigations.
    4.    Airport security full body x-rays very low dose of radiation. It’s in such a low dose that doesn’t reach your baby. Even it doesn’t penetrate beyond your skin.
    5.    Metal detectors, magnetic detectors are completely safe on pregnancy.
    6.    Magnetic Resonance Imaging or MRI is very safe in pregnancy and newborn.
    7.    Airport x-ray screener that is used to see in to our carry-on items doesn’t harm you or unborn baby, though you may be standing close to that.
    8.    X-ray radiation doesn’t get incorporated or impregnated in your clothes that were screened.
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    Epilepsy, or recurrent afebrile seizures, is a pediatric disorder occurring in 5.2 to 7.3 per 1,000 school age children. Fortunately, most children who have a single seizure will not go on to develop epilepsy. Even when they do, the majority will have a relatively benign disorder that can be effectively controlled with a single antiepileptic drug and over time the disorder often resolves itself, allowing the discontinuation of treatment. Proper selection of medication is critical, since all antiepileptic drugs have a potential for significant side effects that may become more severe with higher doses and with polydrug therapy (taking more than one anti-epileptic medication. 
    Despite proper selection of medication and satisfactory compliance, some patients continue to suffer from epileptic seizures. In these children, drug dosages are gradually increased and polydrug therapy is instituted in pursuit of seizure control. Side effects like lethargy, dulled mentation, hyperactivity, aggressivity, double vision, nausea, tremor, and others are to be expected; they must be carefully balanced against the emotional, psychological, and physical consequences of recurring seizures.
    These sequelae are extremely traumatic for epileptic children. Unsure of when the next attack may occur, they are unable to relax, play, and just be kids. In addition, other children often taunt them. The convulsive movements, loss of urinary continence, impairment of consciousness, postictal confusion, and lethargy all create a social stigma that is particularly severe in childhood. Neurosurgery is increasingly being used to treat medically refractory epilepsy, and several centers already offer this treatment.
    Following a detailed documentation of your medical history, our epilepsy team arranges a series of neurological tests to definitively diagnose your condition. We often begin with an electroencephalogram (EEG), which records brain waves through electrodes placed on the scalp. In conjunction with video monitoring, the EEG detects abnormalities in the brain’s “wiring,” or electrical activity. 

    Also available is the complete spectrum of brain scans, including: 
    Computed Tomography (CT) Magnetic Resonance Imaging (MRI) Functional Magnetic Resonance Imaging (FMRI) Positron Emission Tomography (PET) Single Photon Emission Computed Tomography (SPECT) Brain mapping, including grids and depth electrodes Additionally, we offer the WADA test to patients preparing for surgery. This presurgical evaluation maps areas of a patient’s brain that are responsible for such functions as language and memory, for protection during surgery.
    Once a diagnosis has been made, a treatment plan is developed based on your personal needs. The first step is, however, to confirm the seizure diagnosis, as a number of patients may have episodes that are not due to epilepsy. If the diagnosis of epilepsy is confirmed, we frequently start by prescribing antiepileptic drugs, either alone or in combination, as most patients respond to medication. The most common antiepileptic drugs include carbamazepine, valproate or phenytoin, and we also utilize the very latest medications. We also participate in clinical research trials of new medications for seizures. When medications prove ineffective, we can offer a range of other therapies, such as: 

    Vagus nerve stimulation, in which a battery-powered device, implanted in the chest and attached to the vagus nerve in the lower neck, delivers short jolts of electrical energy to the brain, thereby decreasing the frequency of seizures. 

    Ketogenic diet, a medically supervised diet high in fats and low in carbohydrates that has been shown to reduce epileptic episodes in children. 

    Surgery, performed when a lesion, tumor or seizure focus of the brain has been identified as the cause of a patient’s seizures and can be removed. 
    Today most people with epilepsy lead productive, normal lives, with the vast majority controlling seizures and other symptoms with medications alone. Many also are benefiting from special diets and surgical interventions. As researchers continue to introduce advanced diagnostics and new drugs and therapies, those living with epilepsy will be able to further minimize the detrimental effects of their illness and will experience an enhanced quality of life. Our epilepsy services strive to help realize these goals.
    One area of controversy in the field of epilepsy is how to describe the seizures experienced by patients with epilepsy and how to catagorize them in order to sensibly discuss and treat epilepsy. Several congresses have been convined to work on this problem and out of them have come the International Classification of Epilepsies and Epileptic Syndromes. This classificaton has broadly defined seizures as either generalized ("seizures in which the first clinical changes indicate initial involvement of both hemispheres..." or sides of the brain) or partial (location related or focal/local/partial) seizures. 
    Generalized Epilepsy
    Idiopathic Generalized Epilepsies
    These are forms of generalized epilepsies which have a generalized onset involving both sides of the brain. EEG (electroencephalography) recordings of the seizures show bilateral abnormal seizure patterns which are synchronized and symmetrical. Recordings done when no seizures are occurring are normal.
    Benign Neonatal Familial Convulsions
    These are rare seizures which occur just after birth (typically on the 3rd or 4th day of life) and manifest as rhythmic shaking of the body with or without breath holding. This condition is heritable and 14% of these babies will go on to develop epilepsy.
    Benign Neonatal Convulsions
    These seizures usually occur on the fifth day of life for no known reason and are not associated with either a risk for epilepsy or alteration in developmental potential. The convulsion caused shaking of the body and possible brief cessation in breathing.
    Benign Myoclonic Epilepsy in Infancy
    These occur in otherwise normal children during their first or second year of life. The seizures consist of brief jerks of the body or part of it similar to those experienced by most people as they are falling asleep. EEG recordings show brief burst of seizure activity, especially during the early stages of sleep. Later in life a few children who experience this will develop generalized tonic (body stiffening) - clonic (body rhythmically shaking) seizures and children with benign myoclonic epilepsy in infancy can have mild delay in development and minor personality disorders.
    Childhood and Juvenile Absence Epilepsy
    These seizures are associated with a momentary loss of consciousness (frequently not realized by others) with or without abnormal movements or loss of body tone and collapse. The childhood form occurs during early school years, may occur several times a day and are associated with the child later (during teens) developing generalized tonic-clonic seizures (GTCS). The juvenile form usually has an onset around puberty and the events are not uncommonly preceded by GTCSs. The EEG shows bilateral, symmetrical spike-waves which are synchronized and occur at a frequency of 3 per second.
    Juvenile Myoclonic Epilepsy
    Also termed Impulsive Petit Mal Epilepsy, these seizures occur around puberty and consist of single or repetitive jerking which is irregular, arrhythmic and occur bilaterally, predominately in the arms. GTCSs and, infrequently, absences may also occur. The most common time to see the seizures is shortly after awakening or when a person is sleep deprived.
    Epilepsy with GTCS on Awakening
    These seizures occur during the teen years and may be associated with absence or myoclonic seizures. The most common time for the seizures to occur is shortly after awakening from sleep (>90%) but they can also occur in the evening during periods of relaxation. Juveniles with this type of epilepsy will demonstrate a susceptibility to light induced seizures.

    Generalized Cryptogenic or Symptomatic Epilepsies 
    West Syndrome
    Also called Infantile Spasms, this syndrome is manifest by seizures which start in the first year of life and consist of spasms with the body flexing, extending or the head may nod. There is arrest in the baby's development and the EEG has a characteristic pattern (hypsarrhythmia) which is diagnostic. The prognosis for the baby is a function of how well the baby responds to treatment with ACTH or steroids. There are two subgroups of this syndrome 

     Symptomatic Group - The baby has signs of an injured brain (delay in development, signs of abnormal function of parts of the nervous system or MRI/CT scans showing areas of injury in the brain) which predate the onset of the seizures. 

     Cryptogenic Group - There is no known reason for the seizures and examination of the baby is normal.
    Lennox-Gastaut Syndrome
    Children with this syndrome have intractable seizures of multiple types (absence, tonic axial, atonic, myoclonic, GTCS or partial). The frequency of the seizures is high and episodes of status are not unusual. The children exhibit psychomotor retardation and the EEG recordings are characteristic (generalized slow (<2 ½ per second) spike and wave pattern during clinical seizures). This condition can occur in children who had West Syndrome during their infancy. 

    Symptomatic Group - The child has signs of an injured brain (delay in development, signs of abnormal function of parts of the nervous system or MRI/CT scans showing areas of injury in the brain) which predate the onset of the seizures. 

    Cryptogenic Group - There is no known reason for the seizures and examination of the child is normal.
    Epilepsy with Myoclonic-astatic Seizures
    These seizures are mixed and include myoclonic, astatic and myoclonic-astatic seizures in association with absences, GTCS, and tonic seizures as well as non convulsive status. When the status occurs it is usually on awakening and is characterized by apathy or stupor in association with infrequent myoclonus. The onset of this condition is during early childhood and is frequently preceded by a febrile seizure. The EEG has a characteristic evolution over time and the outcome of children with this condition is variable.
    Epilepsy with Myoclonic Absences
    Children with this type of disorder experience absences usually accompanied by severe clonic jerking of both sides of the body. There can also be tonic stiffening of the body during these episodes. These can occur several times during the day. The age of onset is about 7 years and the EEG shows characteristic changes during these episodes which is similar to that seen that seen with childhood absences.
    Symptomatic Generalized Epilepsies and Syndromes
    These occur most commonly in infancy and childhood and the seizures are characterized by generalized seizures and EEG recordings which differ from those described in the idiopathic generalized epilepsies. Not uncommonly the child will exhibit more than one type of seizure and the EEG is characterized by bilateral asymmetrical activity which is less rhythmic than that seen with the idiopathic generalized epilepsies. The child has clinical signs of a diffuse encephalopathy.
    Symptomatic Generalized Epilepsies of Specific Etiologies
    These are seizures which are a prominent feature of a disease or disorder. Malformations of portions of the brain which cause such seizures as infantile spasms. Some malformations can cause characteristic seizures such as hypothalamic hamartomas causing gelastic seizures and infants with tuberous sclerosis commonly exhibiting West Syndrome which evolves into generalized and partial seizures with aging.
    Proven or Suspected Inborn Errors of Metabolism
    These are seizures, generalized or partial, which result when breakdown products of chemical reactions in the body accumulate triggering the seizure or a particular substances important to the normal function of the nervous system cannot be made and the resultant deficit leads to seizures. The seizures may be stereotypic for the condition or may be mixed and the age for onset of the seizures varies with the condition, some starting at birth, some in infancy, some in childhood and some in the teens. There are even a few which do not present until adulthood. A feature of these disorders is they are heritable.

    Generalized Symptomatic Epilepsies of Nonspecific Etiology
    Early Myoclonic Encephalopathy
    The onset of this condition is usually by 3 months of age and starts with myoclonic seizures and evolves to more severe seizures. The EEG recordings show bursts of abnormal activity interspersed with suppression of the brain's normal activity and this pattern evolves into a hysarrhythmia. Babies with this condition arrest in their development as the seizures worsen.
    Early Infantile Epileptic Encephalopathy with Suppression Burst
    This starts during the first few months of life and is characterized by frequent tonic spasms of the body and an EEG recording similar to that seen with Early Myoclonic Encephalopathy. This frequently is associated with developmental arrest or delay and can evolve into West Syndrome by 4-6 months of age.
    Epilepsies and Syndromes Undetermined as to Whether They are Focal or Generalized 
    Neonatal Seizures - These can be difficult to appreciate because of the immaturity of the nervous system. Manifestations of these type of seizures may include such subtle behavior as deviation of the eyes to one side with or without jerking, repetitive movements of the mouth mimicking lip smacking, swallowing, sucking, etc., pedaling or swimming movements in the arms/legs and apneic episodes. Premature infants may exhibit tonic extension in the arms or legs. Infrequently, there can be clonic or myoclonic seizures. These last types have greater significance with regards the baby's prognosis.Severe Myoclonic Epilepsy in Infancy 
    This form of epilepsy evolves out of febrile convulsions, usually in babies with a family history of febrile seizures or epilepsy. The seizures evolve during the first year of life and consist of generalized or unilateral clonic febrile seizures and evolve into myoclonic seizures and partial seizures later. There can be associated psychomotor retardation which becomes more obvious during the second year.Epilepsy with Continuous Spike-wave During Slow-wave Sleep 
    This is an EEG diagnosis with the children exhibiting seizures of varying types during deep sleep (partial or generalized seizures) and also absences while awake. There can be associated neuropsycholgical disorders. 

    Special Syndromes 
    Febrile Convulsions - This is a relatively benign condition seen during early childhood. The seizures are generalized and occur in association with fevers. Usually they are brief but when prolonged there is a chance of injury to the central nervous system which then results in a permanent dysfunction. As only 4% of children having these type of seizures go on to develop epilepsy, routine use of medications to prevent these is unusual unless they become a repetitive problem. 
    Focal or Partial Epilepsy
    These are localization-related epilepsies and syndromes which are referred to as partial, focal or local epilepsies and syndromes. Either the feature or pattern of the seizures or the clinical investigation demonstrate a focal involvement of the brain in these conditions. Patients with these conditions can have a focal area of brain which functions abnormally, has a lesion or tumor or has developed abnormally. The abnormal area is responsible for the abnormal electrical discharges which result in the seizure. Some may have several areas capable of generating abnormal seizures and some may experience a secondary generalization of the seizure activity with the seizure coming to resemble a generalized seizure in very short (within seconds) order after onset of electographic onset of the focal activity. Not uncommonly, the onset may resemble a generalized seizure to a casual observer. In certain types of focal epilepsies (idiopathic age-related focal epilepsies) mirror areas of the two half's of the brain may be capable of generating seizures.
    Focal seizures are commonly described as a function of their point of onset in the brain. To do this a careful history is obtained and extensive EEG recordings coupled with video taping of the patient's behavior are done to better appreciate what the first signs and symptoms of the typical seizure are and how these symptoms and signs progress as the seizure progresses. As a result descriptions of syndromes related to anatomic localization are becoming available.
    Temporal Lobe Epilepsies
    These include simple partial, complex partial and secondarily generalized seizures. The simple partial seizures typically have autonomic (pupillary dilation, flushing in the face, arrest of breathing) and/or psychic symptoms (fear, panic, rage) as well as auditory and olfactory sensations including illusions. The complex partial seizures usually begin with an arrest in motor activity followed by oroailmentary automatism's such as belching, rumbling in the abdomen and then other automatism's follow which typically encompass repetitive, complex movement such as opening and closing a door. The actual seizure usually lasts less than a minute and is followed by confusion and amnesia for a variable period with recovery gradually occurring.
    Temporal lobe seizures can arise from the medial side of the lobe (mesial temporal lobe seizures, limbic seizures, rhinencephalic seizures) or the lateral side (lateral temporal lobe seizures).
    Mesial temporal lobe seizures start deep within the brain so EEGs done between seizures are typically normal. The chances of recording abnormal activity is greatly enhance by using sphenoidal electrodes (thin wire electrodes inserted to lay at the base of the skull below the central part of the brain using thin needles temporarily inserted through the cheek). These seizures usually start with a rising sensation in the abdomen, nausea with autonomic signs and psychic symptoms following.
    Lateral temporal lobe seizures are characterized by auditory hallucinations/illusions, dream like state, disorders in language reception and output and visual symptoms. The seizure can then move to involve the medial temporal lobe, occipital lobe or parietal lobe with onset of corresponding symptoms referable to these areas of the brain.
    Because the memory circuits originate in the temporal lobe, repeated seizure activity which involves these structures can cause difficulties with memory and intellectual function. These seizures typically start in childhood or young adulthood, tend to cluster and are frequently associated with a history of febrile convulsions and/or a family history of seizures.
    Frontal Lobe Epilepsies
    These are generally short, complex partial seizures with minimal or no post ictal confusion. Secondary generalization is common and rapid. Simple partial seizures can also occur. The seizures contain a prominent motor component which is either postural or tonic. At the onset of these seizures complex gestures are common and if the activity spreads to the other half of the brain falling is common.. Given the complex nature of these seizures, they are not uncommonly mistaken for psychogenic seizures. The constellation of signs and symptoms which occur as the seizure starts and progresses offer clues to the site of origin of the seizure. The seizures take their name for the area of the frontal lobe from which they arise. 
    Seizures Types
    Supplementary Motor seizures
    The patient assumes a fencing position with the arms or assumes another posture or exhibits focal, tonic activity. There is speech arrest or vocalizations. 

     Cingulate Seizures - These are complex partial seizures with complex, automatismal gesturing occurring at the onset. Commonly, there are changes in mood and affect and autonomic signs. 
     Anterior Frontopolar Seizures - With these seizures one sees forced thinking, loss of contact with the environment and aversive (movement toward the side of the body opposite side of brain generating seizure) head and eye movement. As these seizures evolve the head and eyes may move back to the side of seizure onset and there may be jerking of the trunk as well as autonomic signs and the patient may fall.
    Dorsolateral Seizures
    Dorso refers to the upper half of the frontal lobe. So these seizures arise in the upper, lateral part of the lobe and typically cause tonic and, occasionally, clonic motor activity with associated versive head and eye movement and speech arrest.
    Orbitofrontal Seizures
    These are complex partial seizures where automatism's (motor and gestural) predominate with olfactory hallucinations/illusions and autonomic signs also occurring. 
    Opercular Seizures
    A primary feature of these seizures are signs and symptoms of alimentary tract involvement including chewing, swallowing, salivation, epigastric sensation, speech arrest, and sound generation. There can be speech arrest, fear and autonomic signs. If the activity spreads secondary sensory changes may occur such as numbness.
    Motor Seizures
    These are usually simple partial seizures and are localized based on what part of the body has movement at the onset of the seizure. If the face's motor region is involved there will commonly be speech arrest, difficulty in swallowing or vocalizations of sounds in association with the tonic or clonic movements of the face's muscles on the side opposite to the area of the brain generating the seizure. These seizures frequently spread (referred to as "marching"; i.e., seizure activity spreads up a arm or leg, marching to involve more and more adjacent muscles). After the seizure there is frequently a weakness for a variable length of time of muscles which were active in the seizure.

    Other Epilepsies
    Parietal Lobe Epilepsies
    These are typically simple partial seizures which can secondarily generalize. Rarely, they can evolve into complex partial seizures. Seizures from this area of the brain typically manifest sensations such as tingling, numbness, loss of the extremity, crawling, coldness or electric sensations in regions of the body but more complex sensations such as feeling that an extremity is moving, or complex alimentary sensations may occur. Rarely, there may be a painful sensation. The involvement may march as with motor seizures of the frontal lobe. There can be complex visual symptoms such as metamorphosis with distortions, foreshortening and elongation may also occur. Severe vertigo or disorientation is a sign of involvement of the lower part of the lobe. If the dominant (usually the left) lobe is involved there can be dysfunction in processing language input and output. These seizures commonly generalize secondarily.
    Parietal Lobe EpilepsiesThese are typically simple partial seizures which can secondarily generalize. Rarely, they can evolve into complex partial seizures. Seizures from this area of the brain typically manifest sensations such as tingling, numbness, loss of the extremity, crawling, coldness or electric sensations in regions of the body but more complex sensations such as feeling that an extremity is moving, or complex alimentary sensations may occur. Rarely, there may be a painful sensation. The involvement may march as with motor seizures of the frontal lobe. There can be complex visual symptoms such as metamorphosis with distortions, foreshortening and elongation may also occur. Severe vertigo or disorientation is a sign of involvement of the lower part of the lobe. If the dominant (usually the left) lobe is involved there can be dysfunction in processing language input and output. These seizures commonly generalize secondarily.
    Occipital Lobe Epilepsies
    There are two categories of Localization-Related Epilepsies or Syndromes with regards their etiology. Each have several subtypes of seizures.
    These are simple partial seizures which commonly undergo secondary generalization. With spread, the seizure can evolve into a complex partial seizure. The initial visual symptoms are usually sparks, flashes or phosphenes but may be scotoma, hemianopsia or amaurosis with the symptoms occurring toward the side opposite the involved part of the brain. There can also be distortion of vision with objects appearing altered in size (too large or small), shape or tilted. Distances may also appear altered. 
    Idiopathic Localization-Related Epilepsies
    These are age-related epilepsies in children whose clinical examinations and testing fail to demonstrate anything other than a focal area of abnormal electrical discharge as recorded by EEG. There is no known causative factor for these children's epilepsies except for a number being hereditarily acquired. These seizures are brief, not associated with neurologic or intellectual abnormalities. The pattern of seizure is generally constant for any given child.

    Benign Childhood Epilepsy with Centrotemporal Spikes
    These are focal seizures commonly occurring around sleep which involve the face, can have a sensory component and can generalize into a GTCS. They are most common in males and can start as early as age 3 and typically burn out between ages 15 and 16. 
    Landau-Kleffner Syndrome is a atypical form of Benign Partial Epilepsy occuring in the speech region of the left frontal lobe.
    Childhood Epilepsy with Occipital Paroxysms
    These seizures start with visual symptoms such as amaurosis, phosphenes, illusions or hallucinations and 25% of patients with this condition will have migraine headache prior to onset of their seizures. The seizure can then spread to involve the posterior temporal lobe and central areas of the brain with onset of behavior which can include clonic activity in one side of the body or complex patterns of body movement. Otherwise, these seizures are very similar to Benign Childhood Epilepsy with Centrotemporal Spikes.
    Symptomatic Focal Epilepsies
    These are epilepsies which are focal in origin and are due to known or suspected disorders of the brain as demonstrated by clinical investigations such as CAT or MRI scans, laboratory testing, etc.
    Chronic Progressive Epilepsia Partialis Continua of Childhood (Kojewnikow Syndrome)
    This is one of the two forms of Kojewnikow Syndrome (the other being Rasmussen's Syndrome) which is a partial motor seizure which can progress to a myoclonic seizure involving the same muscle groups as are involved by the motor seizure. These type of seizures can begin at any age and are usually associated with a demonstrable lesion such as a tumor or vascular abnormality. The seizure disorder will not progress unless the causal lesion does.
    Syndromes Characterized by Seizures with Specific Modes of Precipitation
    These are seizures which reliably result from an environmental or internal factor. A memory or recognition of a specific pattern triggering a complex partial seizure would be an example. Less common would be partial seizures triggered by a simple sensation (a smell, etc.) as such stimulus specific induced seizures are usually generalized. Partial seizures can also be caused by sudden, unexpected arousal, but, again, generalized seizures are more common in this setting.
    What type of testing is used during surgery?
    Intraoperative Electrocorticography
    This localizes precisely the region of seizure focus within the brain. Electrodes either on the surface of the brain or in its depths are used to pick up and record EEG. After resection of the focus is completed, a second recording is done to assure adequacy. These tests can be done on either an awake or anesthetized child.
    Intraoperative Somatosensory Evoked Potentials
    These localize the primary areas of the brain responsible for sensing touch (the postcentral gyrus) and thereby the adjacent region responsible for movement of the body (the precentral gyrus). This test may also be done on an awake or anesthetized child. It is useful not only in identifying motor cortex, but also in establishing landmarks to be used for avoiding injury to cortex important in language processing.
    Intraoperative Cortical Stimulation for Brain Mapping
    This is the type of monitoring typically associated with epilepsy surgery. It may be either gross stimulation of motor cortex to confirm its identity after intraoperative somatosensory recording, or stimulation of cortex to delineate regions important in higher cortical function (e.g., speech centers). While stimulation of motor cortex for purposes of its identification can be done on an anesthetized child, more sophisticated mapping requires an awake, cooperative patient who can communicate with the operative team. For that reason, mapping of the functionally important regions of the brain in children is frequently done outside of the operating room using implanted sheets of electrodes laying on the surface of the brain.
    Implantation of electrodes for localization of seizure focus and brain mapping
    Children frequently require electrode implantation to both precisely localize the focus triggering the seizures and to map regions of the brain important to movement of the body and to speech. Information gained from previous, non-invasive video-eeg monitoring is used to determine what surfaces of the brain must be covered with the electrode sheets. Rarely, a preliminary surgery is required to better define which regions of the brain are responsible for the seizures. In these cases, strips of electrodes are fed through small holes in the skull to accomplish broad coverage over the brain's surfaces. Coverage to define the focus of the seizure is broad so that all borders of the focus can be delineated (typical electrode coverage). Once the site of origin of the seizures has been determined, the electrode sheet is used to map brain function. A surgical plan is then devised using both the map of brain function and the map of site of origin of seizure activity.

    What will be done during surgery?
    Temporal Lobectomy
    The anterior temporal lobe is the most common seizure focus site in patients with partial seizures. Thus temporal lobectomy is the most widely used surgical procedure for epilepsy, and has the greatest rate of success. Approximately 60% of patients become seizure-free, and 85% enjoy a marked reduction of seizures. Behavioral disorders like aggressivity and hyperactivity are often improved.
    Extratemporal Resections
    Seizure foci may be located in the frontal, parietal, or occipital lobes of the brain. Surgical therapy can also be effective for these patients, but the extent of resection is often limited because of important adjacent functional areas. The success rate with extratemporal resections is consequently lower than with temporal ones.
    Multiple Subpial Transections
    This refers to vertical cuts being made through a region of the brain with a seizure focus. Approximately 3/8" of brain must simultaneously discharge to generate a seizure. Nerve fibers which run horizontally through the brain's surface connect this critical mass of brain tissue responsible for initiating the seizure. Nerve fibers which connect the brain with the body run in a vertical direction. Thus, vertical cuts through the brain will transect the fibers important for generating a seizure without disrupting many of the nerve fibers important to the brain's function since these fibers run parallel to the direction of the cut. Cuts are made every 1/4" so that not enough brain tissue is interconnected to generate a seizure.
    Corpus Callosotomy
    This involves the dividing the two major fiber bundles (the corpus callosum and hippocampal commissure) which connect the right and left sides of the brain. The corpus callosum is usually sectioned in two stages: first the anterior two-thirds, and, if seizures persist, the remaining posterior one-third. Candidates for callosotomy are often those who were evaluated for focal resection but have an extensive area, or multifocal areas, of the brain causing the child's seizures. In general, corpus callosotomy is palliative and not curative. It reduces the number of severe seizures and prevents secondary generalization (spread of the seizure activity to involve both sides of the brain with a resultant loss of consciousness) of seizure activity. Thus it reduces the number of injurious falls that occur with the loss of consciousness.
    Subtotal hemispherectomy (either the formal removal of one of the brain's hemispheres or the functional equivalent) is now used to treat medically refractory seizures in patients with pre-existing diffuse hemispheric injury and dysfunction (e.g., infantile spasms and Sturge-Weber). Most of these children have frequent, severe seizures arising from a hemisphere with little or no function, so that the operation does not increase preoperative deficits.
    Seizures must be refractory to medical therapy. Patients should have monotherapy trials with major drugs (i.e., carbamazine, phenytoin, phenobarbital or mysoline, and valporic acid). If these are ineffective or cause intolerable side effects, combination therapy should be tried. Blood testing should be done to insure an adequate amount of the drug is getting into the body. The drug should be escalated until seizures are controlled or unacceptable side effects are encountered. An adequate period of medical therapy is impossible to define precisely. It depends on seizure frequency (more seizures allow the physician to assess efficacy in a shorter period), severity, and whether there are side effects. In most cases where medical therapy is considered to have failed, seizures have been refractory for at least two years.
    Seizures must have a significant adverse effect on the child's life. There is no absolute number of seizures or clinical features that defines intractability. Impairment of consciousness during the waking state is often the critical factor. However, frequent nocturnal convulsions that leave the child lethargic and cognitively impaired the next day are also not acceptable, and would mandate a more aggressive treatment plan. Frequent simple partial seizures that do not cause unconsciousness but disrupt memory function or cause prominent hallucinations and adverse symptoms should be considered for surgical treatment. On the other hand, daytime complex partial seizures in a retarded, institutionalized child may not have a significant adverse effect on the patient's life.
    There are no absolute age limits for this surgery.
    Patients with chronic psychosis and mental retardation are usually not considered.
    Chronic psychosis is not significantly improved by epilepsy surgery. Although the seizures may cease, the patient will remain incapacitated by mental disabilities. Mental retardation (Full Scale IQ of less than 70) indicates diffuse cerebral dysfunction; these children may (1) suffer additional cognitive impairment from surgery, (2) have difficulty cooperating with the extensive presurgical evaluation, and (3) have persistent seizures after the procedure. Surgery for mentally retarded children should be considered only for those who suffer frequent, severe falls in association with seizures. 
    The seizure disorder must be partial.
    Careful history from the patient and from witnesses, in combination with neurologic examination and routine electroencephalography (EEG) will almost always distinguish between partial and primary generalized seizures. In a few cases uncertainty may remain; here video-EEG monitoring is usually diagnostic. Patients with unilateral temporal lobe seizure foci have the best surgical outcome, while those with extratemporal foci do less well. 
    In summary, children with partial seizures that cannot be controlled medically and that disrupt their lives should be considered for surgical treatment.
    Patients must undergo an extensive presurgical evaluation to localize definitely the focus from which the seizures arise. In addition, localization of cerebral function must be performed to identify areas that are critical to cognitive, motor, and sensory functions.
    Surgery should be viewed as another available tool for the management of epilepsy. It is best utilized when partial seizures or medical treatment for them are disrupting a child's development and interpersonal relationships. After surgery, medical management will be greatly simplified, and the seizures will be completely eliminated in a significant number of cases.

    Guillain Barre Syndrome (GBS)

    Guillain-Barré syndrome is a medical emergency, with predominantly motor features; requiring constant monitoring and support of vital functions, often in ITU
    A heterogeneous group of immune-mediated processes characterised by motor (and some sensory, and autonomic) dysfunction. In its classic form, GBS is a rapidly progressive acute inflammatory demyelinating polyneuropathy characterised by a progressive symmetrical ascending LMN muscle weakness, paralysis, and hyporeflexia; with or without sensory or autonomic symptoms Typically, it starts in the lower limb (with reduced tendon reflexes); and progresses into the arms; with mild distal sensory loss. 50% have cranial nerve involvement Most common acquired inflammatory neuropathy. Although the cause is not fully understood, it is thought to be autoimmune; and in most patients, is associated with antecedent infection Several variants. In some, there is an inflammatory demyelinating polyradiculoneuropathy; others affect the axon Diagnosis is clinical; as the classical LP findings (v high protein) may not appear for a week Treatment includes immunoglobulin OR plasma exchange; and, for severe cases, mechanical ventilation Prognosis: 2% mortality; 5-10% require ventilation; 10% cannot walk independently at 1 yr; 30% have some deficit at 3 yrs; 2-5% recur Complete paralysis is compatible with a full recovery Epidemiology/risk factors
    1-2/100,000 pa.  Increased incidence in males. Peak ages: 15-35 and 50-75 yrs  Vaccination Lymphomas - especially Hodgkin's disease Pregnancy - incidence decreases during pregnancy but increases in the months after delivery Variants (6)
    Acute inflammatory demyelinating polyneuropathy (AIDP) - is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an auto-immune response directed against Schwann cell membrane Miller-Fisher Syndrome (MFS) - is a rare variant of GBS and manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS. It usually affects the ocular muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia. There is little significant limb weakness Acute motor axonal neuropathy (AMAN) (or Chinese Paralytic Syndrome) Acute motor sensory axonal neuropathy (AMSAN) Bickerstaff’s brainstem encephalitis (BBE) Acute panautonomic neuropathy Did you know?
    The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and Andre Strohl diagnosed two soldiers with the illness; and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count GBS is also known as: Guillain-Barré-Strohl syndrome; and, Landry’s paralysis, Landry's ascending paralysis, Kussmaul-Landry syndrome, Landry's syndrome, Landry-Guillain-Barré syndrome, Landry-Kussmaul syndrome, acute inflammatory demyelinating polyneuropathy (AIDP), acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis and French Polio Various famous people have had GBS: Joseph Heller, Franklin D. Roosevelt (paralysis long attributed to poliomyelitis), Markus Babbel, William “The Refrigerator” Perry, Tony Benn Aetiology
    In about 2/3rds of patients, the syndrome begins 5 days to 3 wk after a banal infectious disorder, surgery, or vaccination. Infection is the trigger in > 50% of patients Common pathogens include Campylobacter jejuni (especially Penner serogroup 19), enteric viruses, herpesviruses, HIV, cytomegalovirus, Epstein-Barr virus, and Mycoplasma sp A cluster of cases followed the swine flu vaccination program in 1975 Antibodies to ganglioside GM1 are found in 20-30% of cases. There is a strong association with ganglioside GQ1b and the Miller-Fisher syndrome Symptoms
    Can start with paraesthesis in toes; rapidly (hours) followed by LMN symmetrical weakness, usually beginning in the legs; ascends to arms; 90% maximal weakness at 3 wks More marked proximally than distally May involve intercostal or bulbar muscles, or muscles of mastication; causing respiratory failure, dysphasia or dysphagia (can be life-threatening) Muscle wasting develops if axonal degeneration has occurred Sensory complaints; also frequent (less so than motor though) A few patients (possibly with a variant form) have significant, life-threatening autonomic dysfunction causing labile BP, inappropriate ADH secretion, tachycardia, cardiac arrhythmias, disturbed sweating, GI stasis (paralytic ileus), sphincter problems (eg urinary retention), and pupillary changes Muscle/back pain (so differential diagnosis wide); it is important to not make light of the pain a patient with GBS experiences; gabapentin (or a similar neuropathic analgesic) is often required +/- a referral to the ‘pain team’
    Notes: (less commonly): disease affects upper limbs only; or cranial nerves alone; 50% facial and eyelid weakness; sphincter problems rare; can start in head or arms, then progress down; or, sensory symptoms minimal or absent; or asymmetrical; acute onset of bilateral facial palsy is usually due to GBS Key questions
    "When did the weakness start?" "Have you had an infection recently?" Signs
    Fever normally absent Sensory symptoms but limited signs Flaccid paralysis of lower limbs, then upper limbs (usually) Deep tendon reflexes are typically absent; plantars normal Facial palsy (VII), ptosis Tender muscles
    Note: if spinal level, assume spinal cord compresion, until otherwise proven  
    Very high LP protein may not appear for 1 week
    FBC, ESR, CRP U+E, LFTs, Bone, Glucose ± ABG, if hypoxic (on sats) Hep B/C/HIV Protein electrophoresis Other
    LP (usually very high protein, 3-10 g/L; no/few WC; but it may not appear for up to 1 wk and does not develop in 10% of patients) MRI (brain/spine; to exclude other diagnoses) ECG (many different abnormalities may be seen, eg 2nd and 3rd degree AV block, T-wave abnormalities, ST depression, QRS widening, and a variety of arrhythmias) CXR Key Investigation
    LP Specialist Investigations
    Ganglioside antobodies Nerve conduction studies: 
    - Initial testing detects slow nerve conduction velocities and evidence of segmental demyelination in 2/3 of patients
    - However, normal results do not exclude the diagnosis and should not delay treatment
    - Electrophysiologic studies may reveal marked slowing of motor and sensory conduction velocity, or evidence of denervation and axonal loss
    - The time course of the electrophysiologic changes does not necessarily parallel any clinical developments Differential Diagnoses (including all causes of rapid paralysis)
    Neuromuscular (causes of paralysis)
    Brain: brainstem CVA (rapid onset), encephalitis  Spinal cord: spinal cord compression (usually UMN); transverse myelitis (sphincter disturbance and sensory level);  poliomyelitis (LMN; usually occurs in epidemics); tick paralysis (causes ascending paralysis but spares sensation); West Nile virus (causes headache, fever, and asymmetric flaccid paralysis but spares sensation) Peripheral nerve: autoimmune, toxic and metabolic neuropathies (vasculitis, toxins, porphyria)  Neuromuscular junction: myasthenia gravis (intermittent and worsened by exertion); botulism (LMN; may cause fixed dilated pupils (in 50%) and prominent cranial nerve dysfunction with normal sensation) Muscle: hypokalaemia, hyperkalaemia, myositis Non-neuromuscular
    Causes generalised muscle/joint pain (myalgia predominates; eg viral illness)  
    Ventilate sooner rather than later
    Treatment (first line)
    IV NORMAL IMMUNOGLOBULIN 400 mg/kg od, for 5 days; it has some benefit up to 1 month from disease onset (OR plasma exchange) - senior specialist decision SC ENOXAPARIN 40 mg od (prophylaxis) Procedures
    IV line (+ fluids, if dry, or dysphagic) OXYGEN, if hypoxic
    Note: therapy is otherwise symptomatic, the aim being to prevent such complications as respiratory failure or vascular collapse; eg volume replacement or teratment with pressor agents is sometimes required to counter hypotension Nursing issues
    Compression stockings (DVT/PE prevention). Careful nursing, with physio, to prevent pressure sores, chest infection, contractures - and maintain morale Treatment (second line)
    NG feeding, if dysphagic Ventilation (if suspect paralysis ascending to respiratory muscles) Early tracheostomy (muscle activity can take weeks-months to recover) Temporary cardiac pacing (if bradycardic) Prescribing issues
    Steroids of no value Key management decisions
    Immunosuppression Ventilation Admit?
    Yes Bed plan
    Medical admission, then neurology ward ± ITU Referrals
    Neurology ± ITU  
    The Rest
    Don't ignore people when they say they 'cannot walk'. There are several treatable causes (GBS, sc compression, hyperkalaemia etc)
    Urinary retention and extreme constipation can occur; so, catheterise, and pay attention to bowels Respiratory failure (respiratory muscle weakess; 25% patients); 5-10% require ventilation DVT/PE Autonomic dysfunction Follow-up
    Neurology Risk stratification
    Respiratory involvement is very serious Prognosis
    Mortality < 2%.  About 25% of deaths occur during the first week and about 50% during the first month. 10% cannot walk independently at 1 yr Most patients improve considerably over a period of months, but about 30% of adults and even more children have some residual weakness at 3 yr. Patients with residual defects may require retraining, orthopedic appliances, or surgery 2-5% recur; some have further acute episodes; other develop chronic inflammatory demyelinating polyneuropathy 2° Prevention + Health promotion
    Warn about recurrence, and progression to chronic form Don't forget
    Give immunogloblins ASAP Respiratory involvement is serious VENTILATE SOONER > LATER; assess respiratory function 2xday Manage on ITU if any concern Examine regularly (progression) If worried, get MRI to exclude sc compression Complete paralysis compatible with full recovery Red flags
    Respiratory involvement  

    Enterotube II

    Enterotube II is a rapid, multi test kit system used to identify unknown oxidase-negative, gram- negative, rod shaped bacteria from the family Enterobacteriaceae Enterotube II has a tube with a flat side and which contains 12 compartments color coded for different biochemical tests. Enterotube followed by Enterotube II, though improved it’s accuracy, the enterotube II system still may yield false positive or negative results. The Following bacterias can be identified with enterotube test
    Escherichia coil Klebsiella pneumoniae Klebsiella oxytoca Enterobacter aerogenes Enterobacter cloacae Enterobacter agglomerans Serratia marcescens Serraia liquefaciens Serraia rubidaea Providencia stuartii Providencia akcalifaciens Salmonella spp Salmonella phi Citrobacter freundii Citrobacter diversus Proteus mirabilis Proteus vulgaris Morganella morganii Hafitia alvei Enterobacter sakazakii ShigeUa spp Shigella sonnei Edwardsiella tarda Enterotube Tests
    Choose a  well-Isolated colonies from Perti dish, and select one colony for identification. Obtain one Enterotube II and remove the cap from the Enterolube II. Not the bent, but the straight  wire to be used to pick up the bacteria, while the bent end Is the handle. Without flaming  the wire, touch the end to a well-Isolated colony or bocterla from a plate. Avoid touching agar, but try to touch the bacteria only. While gently twisting the wire, pull it through all 12 compartment of the Enterotube II. Now reinsert the wire into the first four compartments (glucose, Lysine, Ornithine and H2S lndole), thereby creating an anaerobic environment.  Break the needle by bending It at the notch, and discard the handle in the breaker of disinfectant. Replace the caps loosely on both ends of the tube. Strip off the blue tape to expose the holes ln the Enterotube II and provide aerobic conditions. Slide the clear plastic band over the glucose compartment any wax that may otherwise escape due to  excessive gas production. Incubate incubated at 37 degrees Celsius for 18-24 hours and then refrigerate it until it is to be observed. Enterotube Results

    Enterotube II interpretation Guide is as under:
    Examine the Enterotube II and interpret all the results except Indole and Vages Proskauer Tests.Results. Once the 24 hours of incubation is complete, all  change in color to be recorded in the manufacturer ID card provided along with the enterotube II interpretation guide. Then reagents are added to the indole and Voges-Proskauer compartments as per the instructions and their results are recorded in the same ID card. The numerical values of the positive tests are added in their appropriate sections to yield a 5-digit ID for the organism being tested. Once the 24 hours of incubation is complete, all  change in color to be recorded in the manufacturer ID card provided along with the enterotube II interpretation guide. Bacterium are attempted to identify with the help of computer generated coding system available on report sheet from the instructor.The instructor will provide directions for the system to determine the ID value to identify the genus and the species of the organism. References :

    Spina Bifida (Myelomeningocele )

    The usual incidence of myelomeningocele, or Spina Bifida, is about one in every thousand live births. While there is no definitive etiology, it seems clear that the pathological process begins before the 4th week of gestation. Neurulation (the normal closing process of the fetus's brain and spinal cord) is normally complete by that time, but it is uncertain whether this disorder represents a failure of neurulation in the base of the spinal cord, or a rupture there after neurulation has become complete. Whatever the cause, there is a defect in the spinal cord's base, with protrusion of the spinal cord and its coverings through a defect in the skin. The condition is often associated with disruption of the cerebrospinal fluid pathways with a resulting hydrocephalus.
    The degree of neurological deficit is directly relates to the level of the spinal cord defect and its extent. If only the bottom of the spinal cord is involved (conus), there may be only bowel and bladder dysfunction, while the most extensive lesions can result in total paralysis of the legs with accompanying bowel and bladder dysfunction. It is because of the varying neurological manifestations of meningomyelocele that there has been so much controversy regarding appropriate treatment.
    Prenatal Detection:
    The overall incidence of meningomyelocele appears to have decreased in recent years, at least in part, because of prenatal testing. Serum alpha-fetoprotein examination (a blood test given to the mother during pregnancy) and ultrasonography can identify a large number of these afflicted fetuses between 16 and 20 weeks. Many parents have then made the decision to interrupt the pregnancy, which is probably why there has been a significant decrease in the number of those born with this anomaly.
    One of the serious questions faced by pediatric neurologists, pediatric neurosurgeons, and obstetricians is how to advise parents of such afflicted babies who seek advice. There is no easy recommendation, it is necessary to weigh a number of issues in an overall assessment of the problem. This is an awesome responsibility for any physician, and there are really no guidelines. If a child has a large lesion, advanced hydrocephalus, and little mobility of the lower extremities, it is easy to predict that neurological function will be severely limited. However, smaller lesions without significant hydrocephalus are a much more difficult problem, even after lengthy discussion, there is often no obvious right or wrong decision. It is a very personal one, and must be made by parents after all the appropriate information is made available to them.
    There have been some differences of opinion as to whether a fetus with known meningomyelocele should be delivered normally or by cesarean section. Advocates of the latter maintain that pressures on the spinal cord during passage down the birth canal may result in irreversible injury and loss of neurological function. Other physicians can find no evidence that this has any bearing on future neurological function, and feel that normal delivery is preferable.
    It is our perspective that there has been no clear-cut, proven benefit of cesarean section, and that both the baby and the parents are better off if delivery is carried out normally.
    Predicting Outcome
    The first question always asked is whether there is permanent brain damage, and if the child will have useful leg function. Unfortunately, the neurologist or neurosurgeon can always predict the minimal expected deficits, but not the maximal ones. If a child is paraplegic (has no movement in the legs from the hips down), one may say with certainty that this patient will always remain in a wheelchair. On the other hand, if the child is born with movement of the thigh muscles and feeling down to below the knees, the chances are good for walking with some sort of brace support. When there are no anomalies of the brain (maldevelopment), it is always possible that intelligence will be normal or above, even if there is advanced hydrocephalus at birth. Thus it is possible to predict for a family how well the child will do, but not how poorly.
    Treatment Options
    The clinical manifestation of meningomyelocele is directly related to the amount of spinal cord involved. As noted earlier, children may have a very wide spectrum of sequelae, ranging from no detectable neurological impairment (other than bowel and bladder), to total paraplegia. In addition, some may be born with a spinal curvature anomaly (either scoliosis or kyphosis), as well as advanced hydrocephalus.
    Much has been written about whether to treat severely afflicted children. Some years ago, John Lorber, M.D., of Sheffield, England, who had enormous early experience in treating children, enumerated what have become known as the "Lorber criteria." According to them, a child born with one of these problems should be excluded from medical or surgical treatment. 1) advanced hydrocephalus, 2) total paraplegia, 3) scoliosis or kyphosis, or 4) an associated anomaly. Dr. Lorber contended that a child with any of these disabilities had a very poor prognosis, and that to prolong that infant's life was, in fact, a disservice. These criteria were employed for some years by North American pediatricians, pediatric neurologists, and neurosurgeons.
    However, it eventually became evident that Dr. Lorber was wrong. He believed that none of these children would survive without treatment, whereas it was the North American experience that about two-thirds of them did. It ultimately turned out that under the British health system at that time, it was common to sedate these children, feed them only on demand, and essentially practice a form of "passive euthanasia." This philosophy was never accepted in North America, with the result that the most afflicted infants not only survived, but were even more disabled through lack of treatment.
    There might conceivably be fewer ethical problems with practicing this sort of selection if to treat equaled life, and not to treat equaled death. But it became obvious that most children survive with or without treatment, so that it was clearly necessary to reassess the overall approach to these unfortunate infants.
    At present time, all children whose parents consent are treated, irrespective of the severity or neurological dysfunction. If parents feel very strongly about withholding treatment, of course, it is generally the position to defer to them. But this rarely happens because from a practical point of view it is impossible to place a child either at home or in custodial care with an open back and a growing head. There is simply no way to arrange any sort of future life without first giving appropriate surgical treatment.
    The basic treatment for meningomyelocele has been well established for many years. The surgeon must replace the neural tissues within the spinal canal and then close the muscle and the skin. A plastic surgeon is occasionally needed if there is a large area that may be difficult to close.
    If there is also significant hydrocephalus, most pediatric neurosurgeons now place a ventriculo-peritoneal shunt at that same procedure. This does not appear to increase the hazard of infection, and it decreases the chance of wound disruption in the lumbosacral region as a result of transmitted spinal fluid pressure.
    Meningomyelocele used to be considered an emergency, and surgery was carried out within a few hours of birth. Nowadays the situation is viewed as urgent but not emergent, in most centers it is considered entirely sufficient to close the back within 2 days of birth. Until then, the tissues are simply kept moist with a saline dressing.
    It is very complicated and difficult to explain all the potential problems associated with meningomyelocele in a single session with a parent. The first question always asked is whether there is permanent brain damage, and if the child will have useful lower limb function. Unfortunately, the neurologist or neurosurgeon can always predict the minimal expected deficits, but not the maximal ones. If a child is paraplegic, one may say with certainty that this patient will always remain in a wheelchair. On the other hand, if the child is born with a L3 or L4 level, the chances are good for walking with some sort of brace support. When there are no anomalies of the brain (maldevelopment), it is always possible that intelligence will be normal or above, even if there is advanced hydrocephalus at birth. Thus it is possible to predict for a family how well the child will do, but not how poorly.
    The basic treatment for meningomyelocele has been well established for many years. The surgeon must replace the neural tissues within the spinal canal and then close the muscle and the skin. A plastic surgeon is occasionally needed if there is a large area that may be difficult to close.
    If there is also significant hydrocephalus, most pediatric neurosurgeons now place a ventriculo-peritoneal shunt (see Hydrocephalus and its Treatment (Shunts)) at that same procedure. This does not appear to increase the hazard of infection, and decreases the chance of wound disruption in the lumbosacral region as a result of transmitted spinal fluid pressure.
    Meningomyelocele used to be considered an emergency, and surgery was carried out within a few hours of birth. Nowadays the situation is viewed as urgent but not emergent, in most centers it is considered entirely sufficient to close the back within 2 days of birth. Until then, the tissues are simply kept moist with a saline dressing.
    Complications of Spina Bifida
    Virtually all babies with meningomyelocele have an associated Arnold-Chiari II malformation, meaning that a portion of the base of the brain (a part of the cerebellum) is displaced down into the spinal canal within the neck. This sometimes causes pressure on the underlying brain stem, which is also elongated and partially within the neck's spinal canal. The most common early symptom of this condition is respiratory stridor, often occurring within 1 or 2 weeks of birth. This usually disappears spontaneously within a few days, or at most three months. It may, occasionally, be associated with impaired function of the lower parts of the brain (difficulty in swallowing, intermittent apnea or cessation of breathing, etc.). In these cases, serious consideration must be given to surgical decompression, a procedure involving removal of the posterior arch of the upper spine over lying the malformation. While this may lead to significant improvement, the results are not uniformly favorable, for it is often the most seriously afflicted infants who suffer from this complication.
    Arnold-Chiari malformation (MRI Scans of AC Malformations) can also cause later neurological deterioration, most often in the adolescent years. It may be associated with intermittent apnea and loss of consciousness (sometimes confused with a seizure). In infants, these cases require a decompressive procedure which must be done on an emergent basis as children with these symptoms are in danger of sudden infant death from apnea. In older children, other symptoms such as suboccipital pain and lower cranial nerve dysfunction may mandate decompression. The results of decompression in this age group are much more favorable than they are in infancy, and the symptoms are completely relieved in most cases.
    In the past few years it has been recognized that a tethered spinal cord may cause progressive loss of function in the lower extremities any time after a child is 3 or 4 years old. Until recently it was assumed that those born with a L3 or L4 level often used a wheelchair as they got older simply as a matter of convenience. It is now understood that every child who has undergone closure of meningomyelocele has a tethered spinal cord, for the neural plate invariably becomes adherent to the surrounding dura. Most patients will probably not develop symptoms, but a significant number of ambulators will gradually deteriorate as a result of this phenomenon. However, if the cord is untethered as soon as symptoms develop, the likelihood of returning to the previous baseline is excellent.
    It has been recognized for several years that rapidly evolving scoliosis may also be associated with a tethered spinal cord, even in the absence of lower extremity function. Therefore, any child with fast-moving scoliosis should have an untethering operation prior to a definitive orthopedicprocedure. If this is done before the scoliosis exceeds 30 degree, there is an excellent possibility of reversal.
    A few of these children will develop hydromyelia (water within the interior of the spinal cord), which is usually manifest clinically by rapidly evolving scoliosis (similar to tethered spinal cord). The hydromyelia may be drained by various techniques (all satisfactory), and the scoliosis will often be arrested.
    Ongoing Treatment
    There are few conditions that require so many specialists to assure the best attainable result. The pediatric urologist, physiatrist, neurologist, orthopedist, and surgeon must all be involved in assessing these children and be involved on a regular basis. It was because of this necessity of multi-disciplinary care that spina bifida clinics evolved in which setting all the specialists are available at a specific time. Thus the child receives optimal care and the parents are spared the necessity of making many different appointments at many different times.
    It is now recognized that at least 70% of children with meningomyelocele have normal intelligence. We now realize, however, that many children who are retarded sustained brain injury simply as a result of a intracranial infection and malfunctioning shunts, in an era in which technology and diagnostic scanning were less sophisticated than they now are.
    Other children died between the ages of 3 and 5 from kidney failure. This danger too is being handled with more advanced methods, particularly intermittent catheterization. In addition, the development of artificial sphincters is progressing well and is expected to be very important in handling urinary incontinency which according to the children themselves, is the most distressing of all the sequelae of meningomyelocele.
    Some 70% of those with this disorder are ambulatory, with or without support. This represents a large number of children who are being integrated into society, mainstreamed in schools, and who are very satisfied with the quality of life they have achieved.
    Achieving Bladder Control in Spina Bifida
    Management of the neurogenic (referring to an abnormally functioning bladder due to compromised nerve supply) bladder secondary to myelomeningocele should be started when a child normally obtains bladder control; however, a baseline urological evaluation should be attained within the first month of life and at regular six month to yearly intervals thereafter.
    A regular bladder routine initially preformed by the patient parents (at about 3 years of age) consists of intermittent clean catheterization performed 3-4 times per day based on the patient's residual urine volume (that amount of urine left in the bladder after the patient voids without the assistance of a catheter) and the bladder's capacity to hold urine. As soon as the patient is cognitively and physically able to perform self-catheterization, instruction should be started with the goal; of independent catheterization. Yearly urological follow-up examinations is imperative in patients with spina bifida to monitor bladder pressure (an indicator of whether the bladder is being stretched by over filling due to excessive intervals between catheterization) as well as bladder capacity, sphincter function (how well the muscle controlling the outlet of the bladder is functioning), and monitoring for bladder or renal stones. Pharmacological agents are prescribed as indicated for high pressure bladder and bladder or sphincter spasticity. Urinary incontinence in a patient on a regular bladder routine is most often due to a urinary tract infection but may also be due to bladder/sphincter dysynergia.
    Control of bowel function in a patient with myelomeningocele is individualized and must be done on a consistent basis. As in starting a bladder routine, a regular bowel routine should be started at about the age of normal bowel continence (~ age three). Prior to the age of beginning a routine, parents should be instructed to modify the child's diet, assure adequate fluid intake and use a laxative as required to prevent constipation over and over distention of the bowels. Bowel management in the child over 3 years of age should be attempted on a daily or every other day schedule. It is best to take advantage of the rectocolic reflex which occurs after eating in the morning or evening as the time of rectal evacuation. An initial combination of a stool softener, irritant cathartic (e.g., ducolax) or peristaltic agent (e.g., Senecot) and suppositories may be tried to establish a regular routine. Modification of the diet as well as the addition of metamucil may be indicated. The end goal is to attain a regular routine without the use of a laxative. Typically, digital stimulation of the rectal outlet is the mechanism used to stimulate evacuation once the routine is established. It must be kept in mind that there cannot be a rigidly prescribed bowel routine which is applicable to all patients - each patient must be tried on a series of medications until a successful bowel routine can be attained.
    Prenatal detection will undoubtedly become more refined, and may well continue to reduce the incidence of meningomyelocele. Another possible advancement that is often discussed concerns intrauterine surgery (surgery on the fetus while still in the womb) to close a meningomyelocele prior to birth. Experimental work has clearly demonstrated that the exposed neural elements are vulnerable to damage from contact with amniotic fluid. There may in fact be progressive loss of lower extremity function during the latter part of gestation. Since this is the case, it would seem reasonable to close the back as early as possible.
    This is certainly attractive from a theoretical point of view. However, in light of the present state of the surgical art, there is, unfortunately, little likelihood that this sort of procedure will be feasible in the foreseeable future.
    The incidence of meningomyelocele has declined as a result of prenatal testing. At the present time virtually all children born with this affliction are treated, irrespective of the magnitude of neurological deficit. This is done because there is simply no way to arrange for future care if the back is open and the head growing.
    It is essential that there be a continuing interchange between parents and physicians to avoid misunderstandings about the complexity of the problem and the necessity of future treatment. But with the assistance of a multitude of specialists, social workers and psychologists, many of these children will have the potential for enjoying an excellent quality of life.