Panayiotopoulos syndrome (PS) is a childhood-related idiopathic benign susceptibility to focal, mainly autonomic, seizures and autonomic status epilepticus.Affected children have normal physical and neuropsychological development. Autonomic manifestations are the cardinal seizure symptoms in PS, and have immense pathophysiological, clinical and treatment implications. All functions of the autonomic system may be affected during the ictus. Nearly half of these seizures last between 30 min and 7 hours, and constitute autonomic status epilepticus.

Mydriasis is sometimes so prominent that it may be reported spontaneously.

Mydriasis occurs concurrently with other marked autonomic manifestations. Dilated pupils may not be reactive to light.

Miosis is rare and occurs with other severe autonomic manifestations while the child is unresponsive.

Hypersalivation is also rare in PS, in contrast to its common occurrence in RS. Combined speech arrest and hypersalivation, as in RS, is even rarer.

Cephalic auras, though rare, are of interest, because they are considered to be autonomic manifestations and because of the diagnostic confusion they may cause with migraine if not properly evaluated. Cephalic auras commonly occur with other autonomic symptoms, mainly nausea, at seizure onset. Occasionally, the child may also complain of “headache” but whether the complaint of “headache” is a true perception of pain, discomfort or some odd sensation in the head is uncertain.

Coughing may occur as an initial ictal symptom either with or without ictus emeticus. It is described as “strange coughing” or “cough as if about to vomit”.

Abnormalities of Intestinal Motility

Diarrhoea (3%) is occasionally reported during the progression of seizures.

 

Figure 9.8 

EEG of a 4-year-old boy with autonomic status epilepticus (more…)

Figure 9.8 

. 

EEG of a 4-year-old boy with autonomic status epilepticus recorded from onset to termination.

Top: High amplitude spikes and slow waves are recorded from the bifrontal regions prior to the onset of the electrical discharge, which is also purely bifrontal (arrow).

Bottom: First clinical symptoms with three or four coughs and marked tachycardia appeared 13 min after the onset of the electrical discharge, when this had become bilaterally diffuse. Subsequent clinical symptoms were tachycardia, ictus emeticus (without vomiting) and impairment of consciousness. No other ictal manifestations occurred until termination of the seizure with diazepines 70 min after onset.

Another lengthy autonomic seizure was recorded on video EEG 1 year later. The onset of symptoms was different with mainly tachycardia and agitation.

From Panayiotopoulos (2004)⁹⁰ with the permission of the Editor ofEpilepsy and Behaviour. Figure courtesy of Dr Michael Koutroumanidis, MD from the Department of Clinical Neurophysiology and Epilepsies, Guy’s & St. Thomas’ NHS Trust, UK.

 

Figure 9.9 

Ictal EEGs in Panayiotopoulos syndrome (top) and Gastaut-type (more…)

Figure 9.9 

. 

Ictal EEGs in Panayiotopoulos syndrome (top) and Gastaut-type childhood occipital epilepsy (bottom).

Top: Samples of continuous EEG recording from the onset to the end of a 9-minute seizure during sleep stage II in an 8-year-old girl. Clinically, the seizure manifested with awakening, eyes opening, frequent vomiting efforts and complaints of frontal headache.¹⁰² The ictal EEG started with remission of the interictal occipital paroxysms and the appearance of occipital sharp rhythms progressing to monomorphic rhythmic theta activity in the bi-occipital regions, but mainly involving the right hemisphere in a wider posterior distribution. The slow activity slowed down with the progress of the seizure and ended without postictal abnormalities. The ECG showed significant tachycardia during the ictus.¹⁰²

Bottom: Ictal EEG during a visual seizure in a boy with Gastaut-type childhood occipital epilepsy. The seizure starts in the left occipital region with fast rhythms associated with visual symptoms. This spreads, 4 s later, to the parietal regions and the child sees a bundle of coloured balloons swinging in his right hemifieId. This lasted for 40 s and was followed by slow waves that progressively became slower and diffuse over the whole brain. At this stage, he complained of clouded vision. This boy was normal physically and intellectually, and also had a normal CT brain scan. At the age of 3 years, he had a nocturnal, left hemiconvulsion. His first EEG showed occipital paroxysms with fixation-off sensitivity. Since the age of 4 years, he had started having frequent, brief visual seizures (simple, coloured, visual hallucinations) provoked by sudden darkness.

From Beaumanoir (1993)¹⁰² and reproduced with the kind permission of the author and the publisher John Libbey

 

Breathing and cardiac irregularities are rarely reported, but may be much more common in a mild form. Breathing changes prior to convulsions include descriptions of “heavy, irregular, abnormal breathing” or “brief cessation of breathing for a few seconds”. Tachycardia is a consistent finding, sometimes at the onset, of ictal EEG (Figures 9.8 and 9.9). 

Cardiorespiratory arrest is exceptional, but is potentially fatal without immediate medical intervention (case 37 in ref⁴).

At the age of 3 years, while dozing in his mother’s car, his head went back, eyes were “rolling”, colour clay-like grey, pupils dilated, unresponsive and incontinent of urine. Arms were initially rigid, but then he became floppy. At this stage, 5–10 min from onset, a Swiss paediatrician who happened to be present diagnosed cardiopulmonary arrest and resuscitated him: “Lips blue and then white. No respiration. No heart beat and wide pupils without reaction to light. External heart massage and mouth-to-nose resuscitation, less than 1 minute. Total time of asystole reckoned to be 2 min. Unconsciousness went on for 20 min then he started to cry and he recognised his mother”. He was well after a few hours’ sleep.⁴

I have been made aware of three other children with PS and cardiorespiratory arrest. Sadly, one of them died. Though tragic and exceptional, this should be expected to happen in view of the frequent occurrence of autonomic status epilepticus in children (page 239).

Ictal Syncope

Ictal syncope is an intriguing and important ictal feature of PS.⁴ It is a common and dramatic occurrence. In at least one-fifth of seizures, the child becomes‘completely unresponsive and flaccid like a rag doll’ before and often without convulsions or in isolation.

Terminology of the Cephalic Auras

Cephalic auras are ictal symptoms of non-specific sensory perceptions involving or limited to the head.⁹¹

While talking to her teacher, suddenly and without warning, she fell on the floor pale, flaccid and unresponsive for 2 min. She had a complete recovery, but 10 min later she complained of feeling sick, vomited repeatedly and again became unresponsive and flaccid with pupils widely dilated for 1 hour. She had an unremarkable recovery and was normal after a few hours’ sleep.

She complained of ‘dizziness’ and then her eyes deviated to the left, she fell on the floor and she became totally flaccid and unresponsive for 5 min.

I proposed the descriptive term‘ictal syncope’^4;90 to describe this state, because‘unresponsiveness with loss of postural tone’ are the defining clinical symptoms of syncope.^92;93 Other authors prefer‘syncope-like symptoms’.⁹⁴

Ictal Behavioural Changes

Ictal behavioural changes usually consist of restlessness, agitation, terror or quietness, which appear at the onset of seizures, often concurrently with emetic or other autonomic manifestations. These symptoms are often similar to those occurring in ‘benign childhood epilepsy with affective symptoms’ (page 254).

He was happily playing and asking questions when he started complaining that he was feeling sick, and became very pale and quiet. He did not want to drink or eat. Gradually, he was getting paler and paler, and kept complaining that he felt sick. He then became restless and frightened. Ten min from the onset, his head and eyes slowly turned to the left. The eyes were opened, but fixed to the left upper corner. We called his name, but he was unresponsive. He had completely gone. We tried to move his head, but this was fixed to the left. There were no convulsions. This lasted for another 15 min when his head and eyes returned to normal and he looked better, although he was droopy and really not there. At this stage he vomited once.

At age 9 years, on return from school, he looked tired and pale. He said that his head was killing him “something that would cause me to be sick”. In 10 min, he started screaming and banging his head on the wall. Within the next 20 min, he gradually became disorientated and floppy ‘like a rag doll’. He was staring.

Conventional Seizure-Symptoms

In PS, pure autonomic seizures and pure autonomic status epilepticus occur in 10% of patients. They start and end solely with autonomic symptoms. In all others, autonomic manifestations are followed by conventional seizure-symptoms and these in order of prevalence are:

• Impairment of consciousness (94%)
• Deviation of the eyes (60–80%)
• Hemiconvulsions (26%)
• Generalised convulsions (20%)
• Speech arrest (8%)
• Visual hallucinations (6%)
• Other manifestations occur less than 3% each.

Impairment of Consciousness

Though initially fully conscious, the child gradually or suddenly becomes confused and unresponsive. Impairment of consciousness may be mild or moderate, with the child retaining some ability to respond to verbal commands, but often talking out of context. Complete unresponsiveness is probably exceptional at the beginning of the seizure. In diurnal seizures observed from onset, clouding of consciousness usually starts after the appearance of autonomic and behavioural symptoms, becoming progressively worse until complete unresponsiveness is reached. Good awareness may be preserved throughout the ictus in around 6% of seizures.

Definition of Ictal Syncope

‘Ictal syncope’ denotes transient loss of consciousness and postural tone that occurs in a seizure before or without convulsions.Transient loss of consciousness and postural tone’ are the defining symptoms of syncope irrespective of underlying cause Ictal syncope is purely a name for a cluster of seizure symptoms that, until now, have lacked a descriptive term. Ictal syncope does not occur or may be very rare in other types of seizures, except in postictal states after GTCS.

Deviation of the Eyes

Unilateral deviation of the eyes with, or rarely without, ictal vomiting is a common ictal manifestation, which seldom occurs at onset. The eyes shift to the extreme of one side and the head may also turn ipsilaterally. This pursuit-like deviation of the eyes may be brief (for min) or prolonged (for hours). It may be continuous or less often intermittent, with eyes returning to the midline and shifting again towards the same side. The eyelids remain open, but may be half open or open wide and, at this stage, consciousness is often, but not invariably, impaired.

Deviation of the eyes may occur without vomiting in 10–20% of patients and, in some children, the eyes may be open wide and remain in the midline before other convulsions occur.

Other ictal symptoms in order of prevalence are speech arrest (8%), hemifacial spasms (6%), visual hallucinations (6%), OPL movements (3%), unilateral drooping of the mouth (3%), eyelid jerks (1%), myoclonic jerks (1%), ictal nystagmus and automatisms (1%). These probably reflect the primary area of seizure discharge generation. The seizures may end with hemiconvulsions often with Jacksonian march (19%) or generalised convulsions (21%).

Ictal visual symptoms, such as elementary visual hallucinations, illusions or blindness, occur after more typical seizure symptoms of PS.

Hemiconvulsive (2%) or generalised convulsive status (2%) is exceptional.

The same child may have seizures with marked autonomic manifestations and seizures in which autonomic manifestations may be inconspicuous or absent. Seizures without autonomic manifestations are rare (7%).⁴

The clinical seizure manifestations are roughly the same irrespective of EEG localisations though there may be slightly less autonomic and slightly more focal motor features at onset in children without occipital spikes.⁴

Seizures without Autonomic Manifestations

Such seizures are rare (7%) and occur in patients who may also have additional autonomic seizures.

Case 3 of ref had three seizures with ictus emeticus. An additional lengthy diurnal seizure manifested only with deviation of the eyes and mild impairment of consciousness prior to generalised convulsions.

Duration of Seizures and Autonomic Status Epilepticus

Nearly half (44%) of the seizures last for more than 30 min and can persist for up to 7 hours (mean about 2 hours), constituting autonomic status epilepticus. The rest of the seizures (54%) last from 1–30 min with a mean of 9 min. Lengthy seizures are equally common in sleep and wakefulness. Even after the most severe seizures and status, the patient is normal after a few hours’ sleep. There is no record of residual neurological or mental abnormalities. The same child may have brief and lengthy seizures. Hemi-convulsive or convulsive status epilepticus is exceptional (4%).

Despite the high incidence of autonomic status epilepticus, convulsive status epilepticus is exceptional in PS.

Circadian Distribution

Two-thirds of seizures start in sleep; the child may wake up with similar complaints while still conscious or else may be found vomiting, conscious, confused or unresponsive.

Clinically, while asleep, “he suddenly got up with both eyes open, vomited several times and then showed a prolonged atonic state with cyanosis and irregular respiration for 3 min” (from ictal EEG documentation by Oguni and associates

The same child may suffer seizures while asleep or awake.

A 10-year-old boy of normal development suffered an episode of autonomic status epilepticus at 5 years of age. Half an hour after he had gone to sleep, he woke up looking pale and then complained that he felt sick before vomiting repeatedly. Within min his eyes deviated and fixed laterally, and soon after he became flaccid ‘like a rag doll’, unresponsive, and incontinent of urine and faeces. His breathing was short and shallow, and stopped for a few seconds before he started vomiting again. Two hours after onset, he had brief hemiconvulsions with Jacksonian marching for 5 min. On arrival at hospital, he was recovering and his temperature was mildly raised to 37.4⁰ C. A CT brain scan, CSF examination and relevant blood tests were normal. Triple treatment for encephalitis was started, though he was entirely normal and apyrexial after a few hours of sleep. EEG the next day showed a few scattered occipital and central spikes. Treatment was stopped 4 days later.

A similar autonomic status epilepticus occurred 6 months later on a ferryboat while on holiday. He said that he felt sick and looked pale. He vomited a couple of times, and then his eyes turned to one side and he talked out of context and vomited again. “Then I knew that he was having another fit” his mother said. “He was as if drifting in and out of sleep. He did not become unconscious, but he was continuously vomiting for several hours.” On arrival at hospital 3 hours later, he was improving and able to talk and walk. He was diagnosed and treated for dehydration. He was normal the next morning. A new EEG showed repetitive multifocal spike-wave complexes.

No further seizures occurred in the next 5 years, and his development and EEG were normal.

Precipitating Factors

There are no apparent precipitating factors other than sleep. Fixation off sensitivity is an EEG phenomenon, which may not be clinically important.

Many seizures have been witnessed while a child is travelling in a car, boat or aeroplane. There are two explanations for this: (a) the seizures are more likely to be witnessed during travelling; or (b), children are more vulnerable because travelling also precipitates motion sickness which is particularly common in children.

Aetiology

PS, like RS, is probably genetically determined. Usually, no family history of similar seizures exists, though siblings with PS or PS and Rolandic epilepsy have been reported. There is a high prevalence of febrile seizures (about 17%). Also, there may be a high incidence of abnormal birth deliveries, but these all need re-evaluation.

PS, Rolandic epilepsy and all other benign childhood focal seizures are probably linked together by a common, genetically determined, mild and reversible functional derangement of the brain cortical maturational process that I proposed to call ‘benign childhood seizure susceptibility syndrome’

Considerations on the Classification of Autonomic Status Epilepticus

Childhood autonomic status epilepticus, though common and specific in childhood, is ignored in all classifications even now, long after its first description by Panayiotopoulos.The new ILAE diagnostic schemerecognises four forms of focal status epilepticus

(a). Epilepsia partialis continua of Kozhevnikov

(b). Aura continua

(c). Limbic status epilepticus (psychomotor status)

(d). Hemiconvulsive status with hemi-paresis

From a clinical point of view aura continua is classified into:

(1) somatosensory, i.e. dysaesthesia phenomena that involve the trunk, head and extremities,

(2) aura continua that involve the special senses (visual, auditory, vertiginous, gustatory and olfactory).

(3) aura continua with predominantly autonomic symptoms, and with psychic symptoms.

It is anticipated that future revisions of the ILAE classifications will recognise this type of age-related autonomic status epilepticus. This is mandated by its high prevalence and its high rate of misdiagnosis and mismanagement. Four-fifths of childhood autonomic status epilepticus occur in PS and the remaining one-fifth occurs in symptomatic childhood epileptic disorders.Ignoring these facts, as indeed happens even now, results in avoidable morbidity and probably mortality.

Pathophysiology

Autonomic symptoms of any type are often encountered in seizures, focal or generalised, in adults or children and they are implicated in occurrences of sudden death. However, autonomic seizures and autonomic status with ictus emeticus and ictal syncope, with the symptomatology and the sequence as detailed in this chapter, are specific in childhood. This clinical picture does not occur in adults: only about 30 cases of ictal vomiting have been reported, but not in the same sequence as in children – adult patients usually have amnesia about the vomiting, which often occurs after the seizure has started with other symptoms (see page 373).An explanation for this is that children are vulnerable to emetic disturbances as exemplified by the ‘cyclic vomiting syndrome’, a non-seizure disorder of unknown aetiology that is also specific to childhood. Ictal syncope is even more difficult to explain.

Symptoms at the onset of seizures are important, because they indicate the possible location of the epileptic focus. However, autonomic and emetic disturbances are of uncertain value with regard to localisation in PS and may occur in seizures starting from the anterior or posterior regions. The localisation of ictal vomiting in adults does not appear to apply in children (page 373).

Clinical and EEG findings indicate that, in PS, there is a diffuse cortical hyperexcitability, which is maturation-related. This diffuse epileptogenicity may be unequally distributed, predominating in one area, which is often posterior. The preferential involvement of emetic and other autonomic manifestations may be attributed to epileptic discharges triggering low-threshold emetic centres and hypothalamus of vulnerable children.In other words, it is likely that in vulnerable children a “weak” epileptic electrical discharge (irrespective of localisation) activates at its onset susceptible autonomic centres to autonomic seizures and autonomic status epilepticus. This is prior to the generation of clinical manifestations from brain regions that are topographically related to the ictal electrical discharge (occipital, frontal, central, parietal and less often temporal) with seizure thresholds higher than those of the autonomic centers.

Diagnostic Procedures

By definition, in an idiopathic syndrome, neurological and mental states and high resolution MRI are normal. The most useful laboratory test is the EEG The most important determinant of the neurodiagnostic procedures is the state of the child at the time of first medical attendance.

• The child has a typical brief or lengthy seizure of PS, but has fully recovered before arriving at the accident and emergency department or being seen by a physician. A child with the distinctive clinical features of PS, particularly ictus emeticus and lengthy seizures, may not need any investigations other than EEG. However, because approximately 10–20% of children with similar seizures may have brain pathology, an MRI may be indicated.
• The child with a typical lengthy seizure of PS has partially recovered, though is still in a postictal stage, tired, mildly confused and drowsy on arrival at the accident and emergency department or when seen by a physician. The child should be kept under medical supervision until full recovery, which is the rule after a few hours of sleep. Then guidelines are the same as above
• The child is brought to the accident and emergency department or is seen by a physician while ictal symptoms continue. This is the most difficult and challenging situation. Symptoms may dramatically accumulate in succession, and demand rigorous and experienced evaluation. A history of a previous similar seizure is reassuring and may help to avoid unnecessary investigation.

Electroencephalography

In about 90% of cases, the EEG reveals functional, mainly multi-focal, high amplitude sharp-slow wave complexes  Spikes may appear anywhere. They are often independent, and occur at various posterior locations and, less often anterior locations, in the same or the contralateral hemisphere, and may appear as cloned-like, repetitive, multifocal spike-wave complexes. In order of prevalence, the complexes most commonly occur in occipital, frontal and centrotemporal regions; right and left regions are equally involved. Midline spikes occur in 17% of cases. 

Occipital paroxysms in their classical form with fixation-off (more…)

Occipital paroxysms in their classical form with fixation-off sensitivity from the initial study of Panayiotopoulos (1981).Top: EEGs from two patients with PS and G-ICOE. In routine EEG, repetitive, high amplitude, occipital sharp and slow wave complexes (occipital paroxysms) occur immediately after the eyes are closed and persist for as long as the eyes remain closed. The EEG normalises immediately after the eyes are opened and for as long as the eyes remain open. The activation of the occipital paroxysms is due to the elimination of central vision and fixation (left of the vertical bar, symbol of eyes with glasses) and inhibition by fixation (right of the vertical bar, symbol of eyes without glasses).

Bottom: Effect of darkness on occipital paroxysms:

(a). Complete darkness activates the occipital paroxysms even when eyes are open.

(b). The occipital paroxysms become continuous in darkness irrespective of whether the eyes are open or closed.

Modified from Panayiotopoulos (1981) and reproduced with the permission of the Editor ofNeurology.

The EEG shows great variability in functional focal spikes at various electrode locations. All brain regions are involved, though posterior areas predominate ( Two-thirds of patients (68%) have at least one EEG with occipital paroxysms or, more commonly, occipital spikes, which are often (64%) concurrent with extra-occipital spikes in at least one EEG.⁴ The other third (32%) never show occipital spikes Instead, they have extra-occipital spikes (21%) only, a consistently normal EEG (9%) or brief generalised discharges only (2%). An EEG with multifocal spikes in more than two, and often many, brain locations occurs in one-third of patients; single spike foci are rare (9%). Cloned-like, repetitive, multifocal spike-wave complexes may be characteristic features when they occur (19%).They have never been studied or reported before in idiopathic epilepsies. On the contrary, multifocal repetitive spikes are considered to be suggestive of a bad prognosis and indicative of symptomatic epilepsies (page 169). Cloned-like, repetitive, multifocal spike-wave complexes do not determine the prognosis, because they occur equally in children with single or multiple seizures.

Spikes are usually of high amplitude and morphologically similar to CTS. They often show stable dipoles in the occipital regions.

Small and even inconspicuous spikes may appear in the same or a previous EEG of children with giant spikes. Though rare, positive spikes or other unusual EEG spike conFigurations may occur.

Brief generalised discharges of slow waves intermixed with small spikes may occur either alone (4%) or more often with focal spikes (15%).

The EEG spikes may be stimulus sensitive; occipital paroxysms are commonly (47%) activated by the elimination of central vision and fixation, while CTS may be elicited by somatosensory stimuli  EEG occipital photosensitivity is an exceptional finding.

Functional spikes in whatever location are accentuated by sleep. If a routine EEG is normal, a sleep EEG should be performed. There is no particular relationship between the likehood of an abnormal EEG and the interval since the last seizure. EEGs recorded a short or long time after a seizure are equally likely to manifest with functional spikes, which may occur only once in serial routine and sleep EEGs.

The background EEG is usually normal, but diffuse or localised slow wave abnormalities may also occur in at least one EEG in 20% of cases, particularly postictally.

Definition of Cloned-Like, Repetitive, Multifocal Spike-Wave Complexes

Cloned-like repetitive multifocal spike wave complexes are repetitive spike or sharp and slow wave complexes that appear concurrently in different brain locations of one or both hemispheres. There may be just two discrete foci unilaterally or contralaterally, but the complexes are usually multifocal and often give the impression of generalised discharges or secondary bilateral synchrony. They are stereotypically and identically repetitive in the same and often subsequent EEGs from the same patient, which is the reason that I coined the name ‘cloned-like’. On the surface, in routine EEG recordings, they appear synchronous but usually one spike focus leads the others by a few milliseconds. The leading focus commonly occurs alone without spikes in other locations. Cloned-like repetitive multifocal spike-wave complexes can occur without the primary spike and can be so abundant that they dominate the EEG and obscure its background, which is otherwise normal. On other occasions, they are scarce and appear in a well-organised EEG with normal background.

EEG abnormalities, particularly functional spikes, may persist for many years after clinical remission; they disappear when the patient reaches the mid-teens. Conversely, spikes may appear only once in one of a series of EEGs.
Frequency, location and persistence of functional spikes do not determine clinical manifestations, duration, severity and frequency of seizures, or prognosis.

Ictal EEG

Typical autonomic seizures and autonomic status epilepticus of PS have been documented by ictal EEG The seizure discharge consists mainly of rhythmic theta or delta activity, usually intermixed with small spikes. Onset is unilateral, often posterior, but may also be anterior and not strictly localised to one electrode. shows autonomic status epilepticus captured from the onset on video EEG. Ictal clinical manifestations may start minutes after the onset of the electrical seizure discharge

Differential Diagnosis

PS is easy to diagnose, because of the characteristic clustering of clinical seizure semiology, which is often supported by interictal EEG findings. However, despite sound clinical EEG manifestations, PS escaped recognition for many years for a number of reasons. Ictus emeticus is rarely considered a seizure event. When it is associated with a deteriorating level of consciousness, followed by convulsions, encephalitis or other acute cerebral insults are the prevailing diagnoses in the acute stage. If the child is seen after complete recovery, atypical migraine, gastroenteritis, motion sickness or a first seizure are likely diagnoses. Similarly, ictal syncope has only recently been recognised as an important clinical manifestation of PS; ictal syncope may be misdiagnosed as cardiogenic syncope, pseudoseizure or a more severe encephalopathic state.

The main problem is to recognise emetic and other autonomic manifestations as seizure events, and not to dismiss them or erroneously consider them as unrelated to the ictus and as a feature of encephalitis, migraine, syncope or gastroenteritis.

EEG of a 10-year-old girl with autonomic seizures and autonomic status epilepticus identical to those of PS (case 60 in ref⁴). The neurological findings and development were normal. However, the EEG had features that were markedly different to the idiopathic cases (rectangle). This prompted an MRI examination, which showed an extensive dysembryoblastic neuroepithelial tumour in the right temporo-parieto-occipital regions, corresponding to severe EEG abnormalities in the same areas.

Since 7 years of age, she had experienced about 10 brief nocturnal seizures lasting 5–10 min each. During these episodes, she jumps out of bed, calls her parents, and complains of feeling sick and of headache. She screams and vomits, her eyes stare and roll, her eyelids blink, her pupils are dilated and she sweats profusely.

A dramatic diurnal autonomic status epilepticus occurred at school. She complained of frontal headache and she had gone out for fresh air when she started feeling “funny”. She screamed that she was hot, and she was sweating and vomiting. Subsequently, she became vacant, her speech slurred slightly, her eyes twitched and she dribbled a lot. She asked for water, but did not drink. She talked “gobbledegook” and gradually got worse. Her head deviated to the left and she became unresponsive. This was followed by a series of left hemiconvulsions lasting 5–10 min each. Convulsions were stopped with intravenous diazepam. She gradually recovered. The neurological examination was normal. She was amnesic of the events the next morning and she looked well, complaining only of photophobia.

The CT brain scan was normal. CSF and other relevant investigations were normal. She received triple therapy for encephalitis for 4 days after which she was discharged home.

 

Similarly, 10–20% of autonomic seizures and autonomic status epilepticus with a similar presentation to PS are due to heterogeneous cerebral pathology, such as focal or diffuse brain lesions of diverse aetiology. These autonomic seizures are also restricted to childhood. In these symptomatic cases, there is often abnormal neurological or mental symptomatology, abnormal brain imaging, and background EEG abnormalities Also, patients commonly have additional types of seizures without autonomic symptoms that continue in adult life. Management and treatment is similar to any other form of lesional epilepsy.

• Gastaut-type idiopathic childhood occipital epilepsy has entirely different clinical manifestations, despite common interictal EEG features when occipital paroxysms occur in PS. Visual seizures are predominant in G-ICOE. Visual symptoms in PS, when present, occur with other typical clinical, mainly autonomic, vomiting and behavioural manifestations. They are not the predominant seizure symptom. They are never the sole symptom of a seizure and do not occur alone. Usually, they develop after the seizure has started. Their presence signifies spreading of the discharge to the occipital regions of the brain. Exceptionally (in 1% of cases), visual symptoms occur at onset suggesting an occipital origin for the epileptic discharge in these patients.
• Rolandic seizures have different clinical manifestations. Emesis, when it occurs, is a concomitant symptom of PS.¹⁴ Conversely, in some cases of PS, there are concurrent Rolandic symptoms. This should not be a problem as the management and the prognosis of both syndromes is the same.
• Cases of PS with seizures occurring when the child is febrile may be diagnosed asfebrile seizures, but this again is of no prognostic significance.

An EEG demonstrating multifocal spikes may be indispensable in the diagnosis of patients with PS if clinical information is inadequate or emetic manifestations are inconspicuous.

Prognosis

PS is a remarkably benign condition despite the high incidence of autonomic status epilepticus. One-third of patients (27%) have only a single seizure, half (47%) have 2–5 seizures and only 5% have more than 10 seizures, which can sometimes be very frequent, but again the outcome is favourable. Furthermore, the active seizure period is very brief and remission commonly occurs within 1–2 years from onset. The risk of developing epilepsy in adult life is probably no more than that in the general population. However, one-fifth of patients (21%) may develop another type of infrequent, usually Rolandic (13%), seizures during their childhood and early teens. These seizures are also age-related and remit before the age of 16 years. Atypical evolutions with absences and drop attacks, such as those occurring in Rolandic epilepsy, are exceptional.

However, despite its benign course, some seizures of PS may occasionally manifest with potentially fatal autonomic symptoms, such as cardiorespiratory arrest.

Management

Current guidelines for febrile seizures, if appropriately modified, may provide the basis for similar guidelines for PS. Based on the risks and benefits of the effective therapies, continuous anticonvulsant therapy is not recommended for children with one or brief seizures. Most clinicians treat recurrent seizures with carbamazepine. Lengthy seizures are a medical emergency and rectal diazepam is prescribed for home administration.

See details in “Management of benign childhood focal seizures” (page 257).

Diagnostic tips
Paediatricians should be alerted by lengthy autonomic seizures and electroencephalographers by frequent multifocal spikes in a normal child with one or a few seizures.
In terms of the EEG, it is important to remember that frequent epileptogenic foci in a normal child with infrequent seizures should raise the possibility of the benign childhood focal seizures.

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This chapter is based on an exhaustive review of the literature regarding all aspects of Rolandic seizures and their EEG manifestations. The history of the ‘discovery of benign Rolandic epilepsy’ has been vividly described by the main French protagonists Marc Beaussart and Pierre Loiseau.

There is no impairment of the cortical language mechanisms. The child is perfectly able to understand what is being said, but unable to utter a single intelligible word. Some authors call thisaphemia oraphonia. However,aphemia means motor aphasia or pure word mutism and does not appear to be correct, andaphonia is an inability to produce sounds by laryngeal mechanisms, which also does not appear to be the case in RS. The arrest of speech in RS is more of ananarthria, that is loss of the power and coordination for the articulation of words, which also explains why this is equally common in left or right sided RS.

Some RS patients are dysarthric rather than anarthic that is they were able to pronounce some words but with difficulty as:

Hypersalivation is one of the most characteristic ictal symptoms of RS and probably occurs in as many as one-third of cases. It is often associated with OPL symptoms, but is also associated with pure hemifacial seizures and may be the most pronounced ictal manifestation. Hypersalivation is not just frothing:

Ictal syncope may occur probably as a concurrent symptom of PS (page 237).

Consciousness is fully retained in more than half (58%) of RS and the patient is able to describe the events after the end of the fits well.

Secondarily GTCS are reported in between one- and two-thirds of children with RS. Primarily GTCS are not part of the syndrome of RS.

Duration of RS is usually brief, lasting for 1–2 min, but may become longer if seizures progress to convulsions.

Circadian distribution. Three-quarters of seizures occur during non-REM sleep, mainly at sleep onset or just before awakening. Seizures during sleep are usually longer and may progress to GTCS, which rarely occurs during wakefulness.

Supported  by
CLINICAL PEDIATRIC ONLINE 

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/

Clinical and Editor in Chief :

WIDODO JUDARWANTO

email : judarwanto@gmail.com,

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

Benign childhood focal seizures and related epileptic syndromes are the commonest and probably the most fascinating and rewarding topic in paediatric epileptology. They affect 25% of children with non-febrile seizures and form a significant part of the everyday practice of paediatricians, neurologists and clinical neurophysiologists who care for children with seizures. Rolandic seizures (RS) are widely recognised and are associated with an excellent prognosis thanks to appropriate research and publications. Paediatricians have been receptive to and have made excellent use of this knowledge. Panayiotopoulos syndrome (PS), a common disorder with dramatic clinical and EEG manifestations, eluded us until recently. PS has now been formally recognised in the new ILAE diagnostic scheme and is becoming more readily diagnosed by physicians. Less common phenotypes, such as the Gastaut type-idiopathic childhood occipital epilepsy (G-ICOE) and idiopathic photosensitive occipital lobe epilepsy have also been recognised and defined. Furthermore, there are also children who manifest with seizures of predominantly affective symptoms, and there are claims of other benign childhood seizures associated with certain interictal EEG foci, such as frontal, midline or parietal, with or without extreme somatosensory evoked spikes.

Supported  by
CLINICAL PEDIATRIC ONLINE 

Yudhasmara Foundation 

JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646 

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/ 

Clinical and Editor in Chief :

WIDODO JUDARWANTO 

email : judarwanto@gmail.com,

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

Clinical Pediatric Neurology concern in newborns, infants, children, and adolescents with a wide range of neurological conditions including epilepsy, muscular dystrophy and other neuromuscular problems, headaches and other pain syndromes, neurofibromatosis and other neurocutaneous syndromes, neurodegenerative disorders, and metabolic disorders. Evaluative tools include electroencephalography (EEG), intensive video EEG monitoring, 24-hour ambulatory EEG, neurosleep studies, evoked potentials, electromyography (EMG) testing and advanced neuroimaging including MRI and high resolution. Staff specialists draw upon the services of many other hospital divisions such as Genetics, Neurosurgery, Developmental Medicine and Behavioral Health.

Typical disorders:

• Seizure disorders and epilepsy
• Muscle disorders, including muscular dystrophy and spinal muscular atrophy
• Migraine and other headaches
• Cerebral palsy
• Developmental delay
• Tics and Tourettes syndrome
• Stroke
• Sleep disturbances (obstructive sleep apnea, insomnia)
• Peripheral nerve disorders such as Charcot-Marie-Tooth

Supported  by
CLINICAL PEDIATRIC ONLINE

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/ 

Editor in Chief :

Dr WIDODO JUDARWANTO

phone : 62(021) 70081995 – 62(021) 5703646, mobile : 0817171764

email : judarwanto@gmail.com 

CLINICAL PEDIATRIC NEUROLOGY, WORKING TOGETHER SUPPORT TO THE HEALTH OF ALL CHILDREN BY RESEARCH, EDUCATION AND INFORMATION NETWORKING. Advancing of the future pediatric to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

CLINICAL PEDIATRIC NEUROLOGY  be a global resource and advocate in the field of pediatric neurology related illnesses and disabilities to maximize their independence and quality of life through neurological knowledge, rehabilitative care, diagnostic testing, and clinical research, advancing excellence in clinical care through education  and information networking

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

• Anatomical Charts

• Atlas of Neuroanatomy With Systems Organization and Case Correlations

• Barr’s The Human Nervous System

• Clinically Oriented Anatomy

• The Human Brain 5e (Nolte)

• The Human Brain in Photographs and Diagrams (2e, Nolte)

• Neuroanatomy 2e, 2nd Edition

• Neuroanatomy and Neurophysiology

• Neuroanatomy through Clinical Cases

Supported  by
CLINICAL PEDIATRIC ONLINE

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/

Clinical and Editor in Chief :

WIDODO JUDARWANTO

email : judarwanto@gmail.com,

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.
Posted in 21.free download-ebooks Tagged: E-BOOK, FREEDOWNLOAD : NEUROANATOMY, PEDIATRIC NEUROLOGY ]]> http://pediatricneurology.wordpress.com/2009/08/19/freedownload-neuroanatomy-pediatric-neurology-e-book/feed/ 1 clinicalpediatric http://pediatricneurology.wordpress.com/2009/08/18/free-download-pediatric-neurology-neurology-and-neuroanatomy-e-books/ http://pediatricneurology.wordpress.com/2009/08/18/free-download-pediatric-neurology-neurology-and-neuroanatomy-e-books/#comments Tue, 18 Aug 2009 09:07:32 +0000 clinicalpediatric http://pediatricneurology.wordpress.com/?p=188 ]]>

• Neuroscience of psychoactive substance use and dependence

• Summary of a Workshop on Research in Multiple Sclerosis

• Anatomy Neuroscience University of Arkansas [English]

• Atlas of EEG Patterns

• Atlas of Epileptic Seizures and Syndromes

• Behavioral Neurology of Movement Disorders

• Child Neurology

• All of a Piece A Life With Multiple Sclerosos

• Alzheimer’s Disease

• Clinical NeurologyI nformation for Professionals

• Cuadernos de Neurologia

• Diagnosis and Management of Dementia

• Disability Determination for Mental Retardation

• eMedicine Neurology

• Furthering Research and Education in Neuropsychopharmacology

• Guia Para Quienes Cuidan Personas con La Enfermedad de Alzheimer

• Guidelines for the Prehospital Management of Traumatic Brain Injury

• La Enfermedad de Alzheimer y Transtornos Relacionados

• La Enfermedad de Alzheimer y Trastornos

• Manual de Alimentacin del Paciente Neurolgico

• Multiple Sclerosis

• Multiple Sclerosis Current Status and Strategies for the Future

• Neuroexam

• Neurologia

• Neurologic Disorders

• Neurology

• Neurology 1

• Practical Guide to Epilepsy

• Primer of EEG With a Mini Atlas

• Principles and Practice of Movement Disorders

• Review Manual for Neurology in Clinical Practice 4E

• Strokes An Illustrated Guide to Brain Structure, Blood Supply and Clinical Signs

• Stroke, 4th Edition

• Surgical Management of Pain

• Vascular Dementia

• Vestibular Function

• Articles Childhood Brain Tumor Foundation [English]

• Basement Page University of Wisconsin Madison [English]

• Basic Information About Brain Tumors Brain Tumor Society [English]

• Basic Neural Processes Tutorials John H. Krantz [English]

• Basic Neurochemistry, Molecular, Cellular, and Medical Aspects Siegel, George J.; Agranoff, Bernard W.; Albers, R. Wayne; Fisher, Stephen K.; Uhler, Mic

• Brain Connection [English]

• Brain Tumor Trials And Treatments [English]

• Brainnet [English]

• Conversations with Neil’s Brain The Neural Nature of Thought and Language William H. Calvin and George A. Ojemann [English]

• Department of Neurology Wake Forest University [English]

• European Dana Alliance for the Brain Brain Information [English]

• Fetal and Young Child Nervous System The Story of the Development and Maldevelopment of the Brain University of Iowa [English]

• Functional Anatomy of Basal Ganglia University of Iowa [English]

• International Brain Research Organization Scientific Issues [English]

• Mathematical Models of Human Memory Tutorials Simon Dennis [English]

• Medical Education American Headache Society [English]

• Merck Manual, Sec. 14, Neurologic Disorders [English]

• Multiple Sclerosis Current Status and Strategies for the Future National Academy Press [English]

• National Institute of Neurological Disorders and Stroke Neurological Disorder Information [English]

• Neurologie CHU de Rennes [Franais]

• Neurologie Lyon Nord F. Mauguire, P. Ryvlin [Franais]

• Neurology eMedicine [English]

• Neurology Family Practice Notebook [English]

• Neurology University of Iowa [English]

• Neuromuscular Disease Center Washington University, St. Louis [English]

• Neuroradiology Teaching Modules Uniformed Services University, Bethesda [English]

• Neurosurgery eMedicine [English]

• Society for Neuroscience Publications [English]

• Traumatic Brain Injury Resource Guide [English]

• Anatomy of the Brain Brain Tumor Foundation of Canada [English]

• Atlas of Brain Perfusion SPECT BrighamRAD [English]

• Atlases of the Brain University of Utah [English]

• BrainInfo A Primate Brain Information System University of Washington Seattle [English]

• Central Nervous System Pathology Index University of Utah [English]

• Comparative Mammalian Brain Collections Wally Welker, John Irwin Johnson, Adrianne Noe [English]

• Cranial Nerves Yale University [English]

• Electronic Human Brain Atlas Northeastern Ohio Universities [English]

• Human Brain Dissections of the Real Brain University of Iowa [English]

• Laboratory of Neuroimaging, University of California, Los Angeles [English]

• Neuroanatomia On Line [Espaol]

• Neuroanatomy and Neuropathology on the Internet, University of Debrecen [English]

• Neuroanatomy Lab Resource Appendices, Temple University [English]

• Neuroanatomy Tutorial, University of Utah [English]

• Neuropathology, Dimitri Agamanolis [English]

• Neuroradiology Teaching File University of Colorado [English]

• Neuroradiology Teaching File University of North Carolina [English]

• Neuroradiology Teaching File Database University of California San Diego [English]

• Neuroradiology Tutor, University of Wisconsin Madison [English]

• Neuroscience, Loyola University [English]

• Skull Module, California State University, Chico [English]

• Spine Surgery [English]

• Synapse Web, Boston University [English]

• Trigeminal Nerve Anatomy, University of Florida [English]

• Tumors of the Pituitary Gland Armed Forces Institute of Pathology [English]

• Whole Brain Atlas, Harvard University [English]

• Neurotransmitter Summary Sheet

• Neurotoxin summary

• Cerebral arteries

• Neuro histology and embryology.

• CNS infections.

• CNS tracts.

• CNS tumors and seizures.

• Neuro pharmacology

• Myelin proteins

Supported  by
CLINICAL PEDIATRIC ONLINE 

Yudhasmara Foundation 

JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/

Clinical and Editor in Chief :

WIDODO JUDARWANTO

email : judarwanto@gmail.com,

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

• Advanced Techniques in Image Guided Brain and Spine Surgery

• Cranial Neuroimaging and Clinical Neuroanatomy

• CT of the Head and Spine

• Imaging Atlas of Human Anatomy, 3rd Edition

• Magnetic Resonance in the Diagnosis of CNS Disorders

• MRI of the Lumbar Spine

• MR Imaging of the Spine and Spinal Cord

• NeuroPET

• Nuclear Medicine in Psychiatry

Supported  by
CLINICAL PEDIATRIC ONLINE 

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/

Clinical and Editor in Chief :

WIDODO JUDARWANTO

email : judarwanto@gmail.com,

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

Supported  by
CLINICAL PEDIATRIC ONLINE

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://clinicalpediatric.wordpress.com/ 

Editor in Chief :

Dr WIDODO JUDARWANTO

phone : 62(021) 70081995 – 62(021) 5703646, mobile : 0817171764

email : judarwanto@gmail.com

Copyright © 2009, Clinical Pediatric Online Information Education Network. All rights reserved.

Clinical Anatomy_ Applied Anatomy for Students and Junior Doct.pdf

Grant’s Dissector.pdf

ANESTHESIOLOGY
Barash Clinical Anesthesia 5th ed.pdf
Miller’s Anesthesia.pdf

BIOCHEMISTRY
Harper’s illustrated biochemistry 26ed.pdf
Harper’s illustrated biochemistry 27th edition.chm
Color Atlas of Biochemistry 2nd Ed J.Koolman K-H. Roehm Thieme 2005.pdf

CARDIOLOGY
ABC of Interventional Cardiology.pdf
Advanced Interventional Cardiology.pdf
Gulizia – Emerging Pathologies in Cardiology.pdf
Cannon – Critical Pathways in Cardiology 2001.pdb
Cardiology cd.exe
Wagner – Marriott’s Practical Electrocardiography 10th ed.pdb

CLINICAL EPIDEMIOLOGY
Basic Epidemiology – Beaglehole , Bonita.pdf
Clinical_Epidemiology__Robert_Fletcher.pdf
Pinciples of Epidemiology, An Introduction to Applied

evidence_base_of_clinical_diagnosis.pdf

Evidence-Based Imaging – Optimizing Imaging in Patient Care.pdf

Evidence-based Medicine Workbook.pdf

Evidence Based Practice in Primary Care [ILLUSTRATED].pdf

DERMATOLOGY
Atlas of Dermatology Schering Co USAss.pdf
Fitzpatrick – Dermatology 5th ed 2005.CHM
Fitzpatrick’s Dermatology In General Medicine 6th ed.pdb
Hall – Sauer’s Manual of Skin Diseases 8th ed.pdb

Handbook of Skin Diseases.pdf

EMERGENCY MEDICINE & ICU
Wolfson – The Clinical Practice of Emergency Medicine 3rd ed.pdb
Pediatric Emergency Medicine. (a comperhensive study guide). 2nd eition,2007.CHM
An Introduction to Clinical Emergency Medicine.pdf
Cline – Emergency Medicine – A Comprehensive Study
Intensive and Critical Care Medicine.pdf
Irwin and Rippe’s Intensive Care Medicine 5th ed.pdb
Noble – Textbook of Primary Care Medicine 3rd ed
Field Guide to Bedside Diagnosis, 2e 2006.CHM.part
Rosen’s Emergency Medicine.chm

ENDOCRINOLOGY
Williams Textbook of Endocrinology 10ed.pdf
Handbook of Diagnostic Endocrinology.pdf

FAMILY MEDICINE & GERIATRICS
CURRENT Diagnosis & Treatment in Family Medicine.chm
Evans – Oxford Textbook of Geriatric Medicine.pdb
Geriatric Medicine An Evidence-based Approach.pdf

HEMATOLOGY & IMMUNOLOGY
Modern Hematology Biology and Clinical Management 2nd ed.pdf
Oxford Handbook of Hematology.pdf
Color Atlas of Hematology.pdf
Wintrobe’s Clinical Hematology 11th.pdb
Adelman – Manual of Allergy and Immunology Diagnosis.pdb
World of Microbiology and Immunology.pdf
HISTOLOGY
Histology Image Review.CHM
Junqueira Carneiro – Basic Histology Text and Atlas 11ed.chm
Kuehnel – color atlas of cytology, histology and microscopic anatomy.pdf

INTERNAL MEDICINE

Harrison’s principles of internal medicine 17ed.chm
Harrison’s principles of internal medicine 16ed.pdf
Harrison_s_Manual_of_Medicine_16th_Edition.pdf
Cecil – Textbook of Medicine.pdf
Kelly’s Textbook of Medicine.pdb
Mayo Clinic Internal Medicine Concise Textbook.pdf
Lippincott.Wilkins.&.Williams.Yamada’s.Textbook.of.Gastroenterology.pdf
Schrier – Manual of Nephrology Diagnosis and Therapy 5th ed.pdb
Bates guide to physical examination+MCQs.pdf

Clinical Interviewing.pdf

Clinical Medicine – 6th edition.pdf

LR – Pocket Medicine 3rd Edition.pdf

Problem Solving in Clinical Medicine.pdf

MICROBIOLOGY
Jawetz, Melnick, & Adelberg’s Medical Microbiology, 24th Ed 2007 McGraw Hill.chm
Laboratory Exercises In Microbiology.pdf
Clinical Microbiology made simple.pdf
The Desk Encyclopedia Microbiology.pdf
Lippincott Illustrated Reviews_Microbiology
Essential Microbiology.pdf
Glazer Microbial Biotechnology – Fundamentals of Applied Microbiology 2nd ed.pdf

World of Microbiology and Immunology.pdf

NEUROANATOMY & NEUROLOGY
Snell’s clinical neuroanatomy
Neuroanatomy An Atlas of Structures, Sections, and Systems – Duane E. Haines.pdf
Adams and Victor’s Principles of Neurology 8th.pdf
Atlas of functional neuroanatomy 2nd ed.pdf

Cranial Nerves Functional Anatomy (2005).pdf

Differential Diagnosis in Neurology and Neurosurgery.pdf

Goetz textbook of neurology.pdb
The Clinical Science of Neurologic Rehabilitation (Contemporary Neurology Series, 66) (2003).pdf
Neuroanatomy – Atlas of Structures Sections Systems 6ed.pdf
Neuroscience – D.Purves, et al.pdf
Merritt – Merritt’s Neurology 10th Ed.pdb
Handbook of Neurology.CHM

Nervous System and Sensory Organs – Color Atlas and Textbook of Human Anatomy – Volume 3.pdf

OBSTETRICS-GYNECOLOGY
Benson Pernolls Handbook of Obstetrics-Gynecology.pdf
Williams Obstetrics 22nd Edition.pdf
Berek & Novak’s Gynecology 14th ed.pdf
Novak’s Gynecology 13ed.pdb
Obstetrics And Gynecology At A Glance.pdf
Stenchever – Comprehensive Gynecology 4th ed – Big Images.pdb
Havens – Manual of Outpatient Gynecology 4ed.pdb
The Johns Hopkins Manual of Gynecology and Obstetrics 2nd ed.pdb

Obstetrics and Gynecology An Illustrated Colour Text.pdf

ONCOLOGY

Weinstein Pediatric Oncology – Pediatric_Lymphomas.pdf

Manual of Pediatric Hematology and Oncology.pdf

Berek Practical Gynecologic Oncology 3ed.pdb

Rosenberg – Cancer – Principles and Practice of Oncology 6th.pdb

Pizzo – Principles and Practice of Pediatric Oncology 4th Ed.pdb

ORTHOPEDICS & RHEUMATOLOGY
MILLER’S_REVIEW_OF_ORTHOPEDICS.pdf
Manual of Rheumatology and Outpatient Orthopedic Disorders Diagnosis and Therapy 4th ed.pdb
Kelley’s Textbook of Rheumatology 6th Edition, 2-Volume Set – ISBN.pdb
DeLee and Drez’s – Orthopaedic Sports Medicine. Editor DeLee (2nd Ed. 2003).pdb
Current Diagnosis & Treatment in Orthopedics 3rd ed.pdb

Pediatric Orthopedics for Primary Care Physicians.pdf

Pediatric Orthopedics in Practice.pdf

PARASITOLOGY
Gillespie & Pearson – Principles and Practice of Clinical Parasitology 2001
Clinical Parasitology.pdf
Dictionary of Parasitology.pdf

PATHOLOGY
Robbins Pathologic Basis of Disease 7th ed 2005.pdf
stedmans Pathology&Lab medicine
Scott_Tietz’s Applied Laboratory Medicine 2nd ed.pdf
Ravel – Clinical Laboratory Medicine – Clinical Applications.pdb

PATHOPHYSIOLOGY OF DISEASE.pdf

PEDIATRICS
Nelson Textbook of Pediatrics 17th ed.pdf
Nelson Essentials of PEDIATRICS.CHM
Current Strategies in Pediatrics 2004.pdf

Pediatric.Musculoskeletal.Disease.pdf

Pediatric.Radiography.3HAXAP.pdf

Treatment.of.Pediatric.Neurologic.Disorders.3HAXAP.pdf

PHARMACOLOGY
Katzung basic clinical pharmacology 10ed.pdf
Katzung basic clinical pharmacology 9ed.pdf
Basic Clinical Pharmacology – 10th Ed.chm
Color Atlas of Pharmacology 3rdEd.pdf

Color Atlas of Pharmacology.pdf
Color Atlas Of Pharmacology,2Nd Ed (By H Lullmann Et Al ,Thieme 2000,Isbn 0865778434).pdf
Lippincott Illustrated Reviews_Pharmacology 2nd ed 2000
Edwards – Principles and Practice of Pharmaceutical Medicine 2nd ed.pdf
Goodman Gilman’s – The Pharmacological Basis of Therapeutics 11th Edition

PHYSIOLOGY
Review of Medical Physiology 21 Edition -William F. Ganong.chm
Physiology – Berne and Levy – 5th Edition.chm
physiology – Guyton.pdf

PSYCHIATRY
Kaplan & Sadock’s Comprehensive Textbook of Psychiatry (2 Volume Set) 7th Ed (Lippincott Williams & Wilkins).pdf
Lewis – Child and Adolescent Psychiatry A Comprehensive Textbook 4th Edition

RADIOLOGY
Dahnert – radiology review manual 4th ed.pdf
Getting Started in Clinical Radiology – from Image to Diagnosis.pdf
Emergency Radiology.pdf
WHO manuals of diagnostic imaging – Radiographic Anatomy and Interpretation of the Musculoskeletal System.pdf
Churchill Livingstone – 2001 – Grainger & Allison’s Diagnostic Radiology. A Textbook of Medical I.pdb

SURGERY
Schwartz Manual of Surgery 8ed.pdf
Oxford Textbook of Surgery (2ed).pdf
Clinical Surgery in General R.M.Kirk 4th Ed 2004.pdf
Wilmore – ACS Surgery – Principles and Practice 2nd ed.zip
Morris – Oxford Textbook of Surgery 2nd ed.pdb
Sabiston Textbook of Surgery, 16th Edition.pdf

Current Surgical Diagnosis and Treatment 11ed With images.pdb
MANUALS, DICTIONARIES, ATLAS
Current Clinical Strategies. Physicians’ Drug Manual. Side Effects, Drug Interactions, and Newly Approved Drugs. 2003 Ed.pdf
Dale – Infectious Diseases The Clinician’s Guide to Diagnosis, Treatment, and Prevention – Big Images.pdb
Bennett and Brachman’s Hospital Infections (Lippincott, 2007).chm
LR – Pocket Medicine 3rd Edition.pdf
Lippincott Williams Wilkins 2003 Medical Terminology An Illustrated Guide 4th Ed.pdf
Merck Manual 17th.Ed.pdb
Pocket Atlas of Radiographic Anatomy 2nd ed, 2000.pdf
Pocket Guide to Diagnostic Tests-0838581358.pdf
Pocket.Guide.to.Musculoskeletal.Diagnosis.3HAXAP.pdf
Oxford Textbook Of Rheumatology, 2nd ed (1998).pdb
Oxford_textbook_of_public_health_4th_ed.pdb
Manual of Clinical Problems In Pediatrics 5th Edition (2000).pdb
Manual of Family Practice 2nd ed.pdb
Ferri’s Clinical Advisor 2004 – Instant Diagnosis and Treatment. 6th edition.pdb
Pocket Atlas of Echocardiography.pdf
Pocket Atlas Of Radiographic Anatomy 2d ed – Torsten B. Moller, Emil Reif.pdf
Pocket_Atlas_of_Human_Anatomy__H._Feneis__W._Dauber._4th_Ed._2000_.pdf
Pocket guide to diagnostic tests.chm
Stedman’s Electronic Medical Dictionary 6th Edition.pdf
Colour Atlas of Anatomical Pathology.pdf
Glossary of Biotechnology Terms, Third Edition.pdf
Clinical Neuropathology Text and Color Atlas.pdf
An Atlas Of Back Pain.pdf
An Atlas of Headache.maxiwarez.pdf
Atlas of Clinical Diagnosis 2nd Ed (2003).pdf
Henry Clinical Diagnosis and Management by Laboratory Methods 21st ed.chm

FLASH CARDS
- ANATOMY (NETTER)
- ANATOMY (ROHEN’S)
- PATHOLOGY
- PHARMACOLOGY

ABC SERIES

ABC of AIDS.pdf
ABC of Antenatal Care.pdf
ABC of Antithrombotic Therapy.pdf
ABC of Arterial and Venous Disease.pdf
ABC of Burns.pdf
ABC of Clinical Electrocardiography.pdf
ABC of Clinical Genetics.pdf
ABC of Clinical Haematology.pdf
ABC of Colorectal Cancer.pdf
ABC of Conflict and Disaster.pdf
ABC of Dermatology.pdf
ABC of Diabetes.pdf
ABC of Eyes.pdf
ABC of First Year.pdf
ABC of Heart failure.pdf
ABC of Intensive Care.pdf
ABC of Interventiona Cardiology 2004.pdf
ABC of Learning Teaching Medicine.pdf
ABC of Nutrition, 4th Edition.pdf
ABC of Occupational and Environmental Medicine.pdf
ABC of Preterm Birth.pdf
ABC of Psychological Medicine.pdf
ABC of Resuscitation.pdf
ABC of Sexually Transmitted Infections.pdf
ABC of Spinal Cord Injury 4th Ed.pdf
ABC of Subfertility.pdf
ABC of the Liver Pancreas and Gall Bladder.pdf
ABC of the Upper Gastrointestinal.pdf

—————————————————————
US MLE REVIEW SERIES

anatomy.pdf
basic epidemiology -beaglehole,bonita.pdf
behavioral sciences.pdf
beyond basic resp.pdf
biochemistry.pdf
clinical anatomy 11ed.pdf
clinical epidimiology -robert fletcher.pdf
kaplan lecture notes.pdf
lecture on visuals.pdf
microbiology,immunology.pdf
pathology.pdf
pharmacology.pdf
physiology.pdf
principles of epidemiology.pdf
Qbook.pdf
upper extremities cadaver pics.pdf
kaplan medical timeline.pdf

OTHERS:

1. Journal Medical Passwords 2003.pdf
——————————————————
1. Anatomy.tv – Anatomy Study Guides.chm
2. Cranial_Nerves_Functional_Anatomy.pdf
3. Outline of Biology – Fried, George H..pdf
——————————————————
1. Gray’s Anatomy for Students.chm
2. Chest Radiology The Essentials, 2nd Edition.CHM
3. Clinical Anatomy by Regions – 8th Ed.CHM
4. Grant’s Dissector.pdf
5. Clinical Radiology Made Ridiculously Simple (MedMaster Series 2003 Ed
6. Clinical Anatomy_ Applied Anatomy for Students and Junior Doct.pdf
7. The Medical Student’s Guide to the Plain Chest Film.pdf
——————————————————
1. Clinical Interviewing 3rd edition.pdf
2. What They Didnt Teach You at Medical School.pdf
3. Medical English.pdf
4. Medical Law and Moral Rights (Springer, 2005).pdf
5. Neuroethics.pdf
——————————————————
1. Ferri’s Clinical Advisor 2008_ Instant Diagnosis and Treatment.CHM
2. Current Medical Diagnosis & Treatment 2007, 46th Ed.chm
3. Handbook of Neurology.CHM
4. Professional Guide to Signs and Symptoms – 5th Ed.chm
5. Colour Atlas of Anatomical Pathology.pdf
6. Glossary of Biotechnology Terms, Third Edition.pdf
7. Clinical Neuropathology Text and Color Atlas.pdf
8. An Atlas Of Back Pain.pdf
9. An Atlas of Headache.maxiwarez.pdf
10. Atlas of Clinical Diagnosis 2nd Ed (2003).pdf
11. Atlas of functional neuroanatomy 2nd ed.pdf
12. Kahle, Color Atlas of Human Anatomy, vol 3 (2003).pdf
13. Neuroanatomy An Atlas of Structures, Sections, and Systems – Duane E. Haines.pdf
14. Pocket Atlas of Echocardiography.pdf
15. Pocket Atlas Of Radiographic Anatomy 2d ed – Torsten B. Moller, Emil Reif.pdf
16. Pocket_Atlas_of_Human_Anatomy__H._Feneis__W._Dauber._4th_Ed._2000_.pdf
17. Stedman’s Electronic Medical Dictionary 6th Edition.pdf
——————————————————
1. Skill 01[1].Temperature..pdf
2. Skill 02[1]..Pulse.pdf
3. Skill 03[1]..Respiration.pdf
4. Skill 04[1]..Blood Pressure.pdf
5. Skill 05[1]..Pulse Oximetry.pdf
6. Skill 06[1]..Capillary Blood Draw.pdf
7. Skill 07[1]..Venipuncture.pdf
8. Skill 08[1]..Blood Draw from a Central Venous Catheter.pdf
9. Skill 09[1]..Nasopharyngeal Swab.pdf
10. Skill 10[1]..Throat Culture.pdf
11. Skill 11[1]..Collection of Stool Specimen.pdf
12. Skill 12[1]..Collection of Urine Specimen.pdf
13. Skill 13[1]..Collection of a Midstream.pdf
14. Skill 14[1]..Assisting with Child during Bone Marrow.pdf
15. Skill 15[1]..Assisting with Child during Lumbar Puncture.pdf
16. Skill 16[1]..Assisting with Collection of Cerebrospinal.pdf
17. Skill 17[1]..Sponge Bath.pdf
18. Skill 18[1]..Insertion of a Peripheral IV Line.pdf
19. Skill 19[1]..Dressing Change Central Venous Line.pdf
20. Skill 20[1]..Insertion of a Nasogastric Tube.pdf
21. Skill 21[1]..Management of Gastrointestinal Suction.pdf
22. Skill 22[1]..Nasogastric Tube Irrigation.pdf
23. Skill 23[1]..Nasogastric Tube Lavage.pdf
24. Skill 24[1]..Administration of a Bolus Feeding.pdf
25. Skill 25[1]..Administration of NG, NJ, Gastrostomy and.pdf
26. Skill 26[1]..Changing a Fecal Ostomy Appliance.pdf
27. Skill 27[1]..Emptying an Ostomy Pouch.pdf
28. Skill 28[1]..Administration of Enemas.pdf
29. Skill 29[1]..Urinary Catheterization.pdf
30. Skill 30[1]..Petaling a Cast.pdf
31. Skill 31[1]..Pin Site Care.pdf
32. Skill 32[1]..Care of the Child in an External Fixation.pdf
33. Skill 33[1]..Pin Care, External Fixation Device.pdf
34. Skill 34[1]..EVD Maintaining System at Correct Level and Functioning.pdf
35. Skill 35[1]..EVD Client Assessment.pdf
36. Skill 36[1]..EVD Monitoring Cerebrospinal Fluid (CSF).pdf
37. Skill 37[1]..EVD Changing the Drainage Bag.pdf
38. Skill 38[1]..EVD General Nursing Care and Safety.pdf
39. Skill 39[1]..Assisting with Chest Tube Insertion.pdf
40. Skill 40[1]..Preparing the Chest Tube Drainage System.pdf
41. Skill 41[1]..Care of the Child with a Chest Tube.pdf
42. Skill 42[1]..Assisting with Removal of Chest Tube.pdf
43. Skill 43[1]..Oxygen Administration.pdf
44. Skill 44[1]..Bulb Suctioning.pdf
45. Skill 45[1]..Nasotracheal Suctioning.pdf
46. Skill 46[1]..Tracheostomy Monitoring.pdf
47. Skill 47[1]..Tracheostomy Tube Change.pdf
48. Skill 48[1]..Tracheostomy Tube.pdf
49. Skill 49[1]..Tracheostomy Suctioning.pdf
50. Skill 50[1]..Endotracheal Tube Monitoring (ETT).pdf
——————————————————

Churchill Livingstone – 2001 – Grainger & Allison’s Diagnostic Radiology. A Textbook of Medical I.pdb
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clinical_evidence_vol_9.pdb
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Color Atlas of Physiology.pdf
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Encyclopedia of Infectious Diseases.pdf
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Evidence Based Practice in Primary Care [ILLUSTRATED].pdf
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Evidence-based Medicine Workbook.pdf
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Fractures_in_children_5ed.pdb
Functional Neuroanatomy of Pain.pdf
General Practice, 3rd Edition (J. Murtagh).pdb
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Hand Bone Age.pdf
Handbook of couples therapy.pdf
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How to Read a Paper.pdf
Human Biology_0071218068.pdf
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Information Technologies in Medicine – Volume I.pdf
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Interpretation of Diagnostic Tests 7th ed.pdb
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Lab Notes Guide to Lab and Diagnostic Tests (2005).pdf
Learning_Medicine_An_Informal_Guide_to_a_Career_in_Medicine.pdf
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Managing the symptoms of multiple sclerosis.pdf
Managing Your Multiple Sclerosis.pdf
Manual of Clinical Problems In Pediatrics 5th Edition (2000).pdb
Manual of Family Practice 2nd ed.pdb
Manual of Rheumatology and Outpatient Orthopedic Disorders Diagnosis and Therapy 4th ed.pdb
Marketing health services.pdf
Massage For Dummies.pdf
MCQ.Companion.to.Applied.Radiological.Anatomy.3HAXAP.pdf
Means Ends and Medical Care.pdf
Medical and Psychosocial Aspects of Chronic Illness and Disability, Third Edition (2005).pdf
Medical Malpractice – A Physician’s Sourcebook.pdf
Medical_Physiol_2nd_Ed.pdf
Merritt – Merritt’s Neurology 10th Ed.pdb
MILLER’S_REVIEW_OF_ORTHOPEDICS.pdf
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Nelson.Textbook.of.Pediatrics.17th.ed – Behrman.pdb
Nervous System and Sensory Organs – Color Atlas and Textbook of Human Anatomy – Volume 3.pdf
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Neurotransmitters, Drugs and Brain Function Wiley (2001).pdf
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Occupational Health Practice – Arnold.Publishers.Fourth.EditionISBN0750627204.pdf
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Outpatient and Primary Care Medicine, 2005 Edition (2004).pdf
Oxford Textbook Of Rheumatology, 2nd ed (1998).pdb
Oxford_Dictionary_of_Medical_Quotations.pdf
Oxford_textbook_of_public_health_4th_ed.pdb
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Pediatric Radiography.pdf
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PATHOPHYSIOLOGY OF DISEASE.pdf
Pediatric Orthopedics for Primary Care Physicians.pdf
Pediatric Orthopedics in Practice.pdf
Physical Medicine and Rehabilitation Board Review.pdf
Pocket Atlas of Radiographic Anatomy 2nd ed, 2000.pdf
Pocket Guide to Diagnostic Tests-0838581358.pdf
Pocket.Guide.to.Musculoskeletal.Diagnosis.3HAXAP.pdf
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Rosen’s Emergency Medicine.chm
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Soft Tissue Rheumatology.CHM
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Textbook of Clinical Trials Wiley (2004).pdf
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