Encephalitis is inflammation of the brain parenchyma that is usually caused by viral infection. Common viruses include herpes simplex virus type 1 and West Nile virus. Clinical features include altered mental status, seizures, and focal neurological deficits. Diagnosis involves CSF analysis showing pleocytosis and identifying the virus through PCR or serology. Treatment involves antivirals for suspected viruses and managing increased intracranial pressure and seizures. Prognosis depends on the specific virus and early initiation of treatment.
respiratory inspections are common in elderly people and often times,that tickles into the lungs.More often than not they have comorbiidites,like Diabetes,hypertension etc.Hence,the treatment has to be different and some times the prognosis is guarded
the scenario given at the start of ppt z nt interstitial lung diseases... its a similar diseases to it.... diagnose it urself to differniate it and hv better command over diffferntial diagnosis.
respiratory inspections are common in elderly people and often times,that tickles into the lungs.More often than not they have comorbiidites,like Diabetes,hypertension etc.Hence,the treatment has to be different and some times the prognosis is guarded
the scenario given at the start of ppt z nt interstitial lung diseases... its a similar diseases to it.... diagnose it urself to differniate it and hv better command over diffferntial diagnosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
3. Definition
Encephalitis is the Generalized inflammation
of the brain parenchyma
The term encephalitis indicates that the
predominant clinical syndrome arises from
infection and inflammation in the parenchyma
of the brain rather than in the leptomeninges.
4. Introduction
Viral infections of the central nervous system result in
the clinical syndromes of aseptic meningitis or
encephalitis.
The true incidence of these infections is difficult to
determine because many cases are unreported, the
diagnosis may not be considered, or a specific viral
etiology is never confirmed.
However, these disorders occur with sufficient
frequency that clinicians should be familiar with the
clinical manifestations, diagnostic techniques, and
5. Epidemiology
The reported incidence for acute encephalitis
varies worldwide but is generally between 3.5
and 7.4 cases per 100,000 patient years.
Incidence of 7.4 per 100,000 person-years in
Minnesota, USA in people of all ages.
whereas a lower rate of 1.5 per 100,000
population was reported in England.
Incidence tends to be higher in the paediatric
population compared to adults (Granerod & Crowcroft,
6. VIRAL PATHOGENS
The most commonly identified viruses causing sporadic
cases of acute encephalitis in immunocompetent adults is
herpes simplex virus type 1
Eastern Equine Encephalitis and western equine
encephalitis virus
WNV
St. Louis encephalitis virus north America
Japanese encephalitis virus in Asia and the western Pacific
California encephalitis virus serogroup
La Crosse virus
7.
8. The mechanisms involved in viral transport from the
circulation to the brain are not clearly understood.
However, it is clear that transendothelial passage of the
virus occurs in vessels of the choroid plexus, meninges,
or cerebrum by one or more of the following
mechanisms
Bridging the endothelium within migrating leukocytes
Breaking through damaged endothelium
9. Pathogenesis
• HSV is a DNA virus :
– nuclear invasion
– DNA replication
– DNA expression & protein production
• Host cell lysis
• Virus spread & mutiple cell type infection (panencephalitis)
• MHC expression and immune system recruitment
• Massive inflammatory response
• Oedema and Necrosis
• Detersion
10.
11. Clinical manifestation
the patient with encephalitis commonly has an altered
level of consciousness (confusion, behavioral
abnormalities)
Hallucinations, agitation, personality change,
behavioral disorders, and, at time a frankly psychotic
state.
Focal or generalized seizures occur in many patients
12. The most commonly encountered focal
findings are aphasia, ataxia, upper or lower
motor neuron patterns of weakness, involuntary
movements (e.g. myoclonic jerks, tremor) , and
cranial nerve deficits (e.g. ocular palsies, facial
weakness) .
Involvement of the hypothalamicpituitary axis
may result in temperature dysregulation,
diabetes insipidus, or the development of the
syndrome of inappropriate secretion of
13. Parotitis strongly suggests the diagnosis of mumps
encephalitis in an unvaccinated patient with mental status
changes.
Flaccid paralysis that evolves into an encephalitis strongly
suggests the possibility of West Nile virus infection . In fact,
it has been misdiagnosed as Guillain-Barré syndrome.
A maculopapular rash is also seen in approximately half of
patients with this infection and is not expected in other viral
encephalitides.
14. Tremors of the eyelids, tongue, lips, and extremities
may suggest the possibility of St. Louis encephalitis or
West Nile encephalitis.
Findings of hydrophobia, aerophobia, pharyngeal
spasms, and hyperactivity suggest encephalitic rabies.
Grouped vesicles in a dermatomal pattern may suggest
varicella zoster virus (VZV), which can occasionally cause
encephalitis.
15. Diagnosis
Imaging
oCT scanning is useful to rule out space-
occupying lesions.
oMRI is sensitive for detecting demyelination,
which may be seen in other clinical states
presenting with mental status changes (eg,
progressive multifocal leukoencephalopathy).
17. CSF Examination: characteristic CSF profile is
indistinguishable from that of viral meningitis and
typically consists of a lymphocytic pleocytosis, a mildly
elevated protein concentration, and a normal glucose
concentration.
A CSF pleocytosis (>5 cells/μL) occurs in >95% of
immunocompetent patients with documented viral
encephalitis.
In rare cases a pleocytosis may be absent on the
LP but present on subsequent LPs.
18. CSF PCR: The most important viral etiology to rule out in a
patient with encephalitis is HSV, Diagnosis is most readily
made by detecting HSV DNA by PCR on CSF
Enteroviruses are more commonly associated with viral
meningitis, but infrequently they may cause encephalitis as
well.
PCR testing on the CSF sample is the diagnostic test of
choice.
The pathogen can also be cultured from the stool and
19. Serology.
the presence of IgM antibodies in a single serum provides
presumptive evidence of St. Louis encephalitis
West Nile a single specimen looking for IgM antibodies in
the serum or CSF is sufficient for diagnosis.
A single serum specimen can also be used to diagnose
mumps.
Serology may also be helpful in obtaining evidence for
primary Epstein-Barr virus infection, a rare cause of
meningoencephalitis.
20. Brain biopsy — As a last resort, brain biopsy
can be considered in the patient if the etiology
of encephalitis is still unknown.
Herpes simplex virus: culture of suspicious
and a Tzanck smear should be obtained.
22. EMPIRIC THERAPY
oThere are no specific therapies for most central nervous
system (CNS) viral infections.
oEmpiric treatment for herpes simplex virus (HSV) -1
infection with acyclovir (10 mg/kg intravenously every
eight hours).
oEarly therapy is vital because it is associated with a
significant decrease in mortality and morbidity.
Acyclovir should also be considered if varicella zoster
virus encephalitis is likely.
23. INCREASED INTRACRANIAL PRESSURE
Cerebral edema
Elevate head of the bed
Frusemide iv 20mg
Mannitol 0.25 to 1 g/kg bolus every 4–6 hours
Dexamethasone iv 10 mg q6h helps in
managing edema surrounding SOL
Hyperventilation
24. Seizures and status epilepticus
First line,
initial dosing Lorazepam 0.1 mg/kg IV up to 4 mg per dose.
Midazolam 0.25 mg/kg IM up to 10 mg maximum. Diazepam
0.15 mg/kg IV up to 10 mg per dose
Second line,
initial dosing Fosphenytoin 20 mg PE/kg IV. Levetiracetam
1,000–3,000 mg IV. Valproate sodium, 20–40 mg/kg IV
Third line,
loading dose Propofol 1–2 mg/kg. Phenobarbital 20 mg/kg IV.
Pentobarbital 5–15 mg/kg IV
25. PROGNOSIS
Most studies of viral encephalitis are focused on short-
term outcomes.
The most frequent sequelae included difficulties in
concentration, behavioral and speech disorders, and
memory loss.
One-quarter of those who were previously employed
had not returned to work.
26. PARANEOPLASTIC ENCEPHALITIS
Paraneoplastic encephalitis may manifest as
limbic or brainstem encephalitis.
In the majority of cases, symptoms have an
acute to subacute onset.
cerebrospinal fluid (CSF) often shows
abnormalities such as pleocytosis, increased
protein concentration, oligoclonal bands.
elevated immunoglobulin G (IgG) index,
suggesting an inflammatory process.
27. AUTOIMMUNE ENCEPHALITIS
The autoimmune encephalitis syndromes have
a wide clinical spectrum that ranges from
typical limbic encephalitis to syndromes.
Neuropsychiatric symptoms such as deficits of
memory, cognition, psychosis, seizures,
abnormal movements, or coma.
This group of disorders is associated with
antibodies to neuronal cell surface/synaptic
proteins
28.
29. The target antigens usually play critical roles in
synaptic transmission and plasticity.
While patients are often severely affected
these disorders are highly responsive to
immunomodulatory therapies.
As early initiation of treatment (immunotherapy
and tumor-directed therapy, if present) has been
shown to improve outcomes, speed recovery.
31. INTRODUCTION
Brain abscess is a focal collection within
the brain parenchyma, which can arise as
a complication of a variety of infections,
trauma, or surgery.
32. Epidemiology
1500-2500 cases per year in the US
8% of ICSOL in developing countries
Male Female ration = 2-3 : 1
Median age – 30 – 40 yrs
• 2° to otitic focus - <20 / > 40 yrs
• 2° to PNS infection – 30-40 yrs
25% in children – otitic focus / CHD
0.2% of cranial operations
Immunosuppression
33. Etiology
The most frequent causes of brain abscess
are Streptococcus and Staphylococcus spp
Viridans streptococci and Staphylococcus
aureus are the most common
The pathogens involved differ depending upon
the site of the primary infection, the age of the
patient and the immune status of the host.
37. PATHOGENESIS
Direct spread — The direct spread of organisms from a
contiguous site usually causes a single brain abscess.
Primary infections that can directly spread to the
cortex include:
Subacute and chronic otitis media and mastoiditis
(spread to the inferior temporal lobe and cerebellum)
Frontal or ethmoid sinuses (spread to the frontal
Dental infection (usually spreads to the frontal lobes)
38. Bullet wounds to the brain can result in
necrotic tissue and leave metal fragments that
can serve as a nidus for infection.
Other foreign bodies that have been
associated with brain abscesses include a pencil
tip lodged in the eye and a lawn dart.
Brain abscess can also complicate
neurosurgical procedures.
39. Hematogenous spread
Brain abscesses associated with bacteremia
usually result in multiple abscesses that are
most commonly located in the distribution of
the middle cerebral artery
Abscesses usually form at the grey-white
matter junction where micro infarction
damages the blood-brain barrier.
40. Pathology
The early lesion (first one to two weeks) is
poorly demarcated and is associated with
localized edema. There is evidence of acute
inflammation but no tissue necrosis. This early
stage is commonly called cerebritis.
After two to three weeks, necrosis and
liquefaction occur, and the lesion becomes
surrounded by a fibrotic capsule.
41.
42.
43. CLINICAL MANIFESTATIONS
The manifestations of brain abscess initially
tend to be nonspecific
the classic triad of headache, fever, and focal
neurologic deficit is present
This always result in a delay in establishing the
diagnosis.
44. Symptoms
Headache is the most common symptom of a
brain abscess.
The pain is usually localized to the side of the
abscess, and its onset can be gradual or
sudden.
The pain tends to be severe and not relieved
by analgesics.
45. Neck stiffness occurs in 15 percent of patients with
brain abscess.
changes in mental status (lethargy progressing to coma)
are indicative of severe cerebral edema and are a poor
prognostic sign.
Vomiting generally develops in association with
increased intracranial pressure.
46. Physical examination
Focal neurologic deficits are observed in up
50 percent of patients and generally occur
to weeks after the onset of headache
Seizures develop in 25 percent of cases and
can be the first manifestation of brain abscess
Third and sixth cranial nerve deficits indicate
raised intracranial pressure.
47. DIAGNOSIS
In the setting of focal symptoms (eg, unilateral
headache) or signs (eg, unilateral cranial nerve
deficits, hemiparesis) or the finding of
papilledema, a lumbar puncture (LP) is
contraindicated.
Computed tomographic (CT) scan with
contrast or magnetic resonance imaging (MRI)
should be performed prior to LP in this
48. Computed tomographic scan
Early cerebritis appears as an irregular area of low
density that does not enhance following contrast
injection.
As cerebritis evolves, the lesion enlarges with thick
diffuse ring enhancement following contrast injection.
The ring of contrast enhancement represents
breakdown of the blood-brain barrier and the
49.
50. Magnetic resonance imaging
Is more sensitive for early cerebritis
Is more sensitive for detecting satellite lesions
More accurately estimates the extent of
necrosis, ring enhancement, and cerebral
edema
Better visualizes the brainstem
Is capable of differentiating ring-enhancing
lesions due to brain abscess from neoplastic
lesions
51.
52. Lumbar puncture
Rarely, the CSF formula resembles bacterial
meningitis, which indicates rupture of the
abscess into the ventricle
When this occurs, the PMN count can be
higher than 150,000/microL with
hypoglycorrhachia and an elevated protein.
53. Culture
The specimen obtained from stereotactic CT-
guided aspiration or surgery should be sent
Gram stain, aerobic, anaerobic, mycobacterial,
and fungal culture.
In addition, special stains including an acid-
stain for mycobacteria, modified acid-fast stain
for Nocardia, and fungal stains should be
performed to aid in the identification of the
54. •Histopathology
Definitive diagnosis of brain abscess
and, frequently, the identification of
the etiologic agent are made by
pathologic examination of brain
tissue obtained by open or
stereotactic brain biopsy.
55. Laboratory investigations
TC – Normal / mild ↑ (↑ if meningitis / acute
systemic infection)
ESR - ↑ in >90%
CRP - ↑. Useful marker to differentiate
between brain abscess and slowly progressive
ICSOLs
Blood culture - +ve in IE / mycotic aneurysms
CSF analysis – Non-specific.
Mild pleocytosis. CSF potein – mild ↑
Glu – Normal
LP – dangerous
PCR analysis of 16S rDNA – to identify to
species level
111In-labelled leukocytes
56. THERAPY
Successful management of a brain abscess
usually requires a combination of antibiotics
and surgical drainage for both diagnostic and
therapeutic purposes
57.
58. Empiric therapy
For patients with a brain abscess arising from
an oral, otogenic, or sinus source
Metronidazole (7.5 mg/kg [usually 500 mg]
every six to eight hours) PLUS either
ceftriaxone (2 g IV every 12 hours) or
cefotaxime (2 g IV every four to six hours).
59. For patients with a brain abscess from
hematogenous spread
Vancomycin (15 to 20 mg/kg per dose IV
every 8 to 12 hours, not to exceed 2 g per
dose) for empiric coverage of MRSA.
If susceptibility testing reveals methicillin-
sensitive S. aureus, vancomycin should be
replaced with nafcillin (2 g IV every four
hours) or oxacillin (2 g IV every four hours).
60. For brain abscess in postoperative neurosurgical
patients, we recommend treatment with:
Vancomycin(15 to 20 mg/kg per dose IV every 8 to 12 hours, not
to exceed 2 g per dose) PLUS ceftazidime(2 g IV every eight
hours), cefepime(2 g IV every eight hours), or meropenem(2 g IV
every eight hours).
For brain abscess following penetrating trauma, we
recommend treatment with:
Vancomycin(15 to 20 mg/kg per dose IV every 8 to 12 hours, not to
exceed 2 g per dose) PLUS ceftriaxone(2 g IV every 12
hours) or cefotaxime(2 g IV every four to six hours).
61. For brain abscesses with an unknown source,
we recommend treatment with:
Vancomycin (15 to 20 mg/kg per dose IV every 8 to 12 hours,
not to exceed 2 g per dose) PLUS Metronidazole (7.5 mg/kg
[usually 500 mg] IV every six to eight hours) PLUS Ceftriaxone
(2 g IV every 12 hours) or cefotaxime (2 g IV every four to six
hours). Cefepime (2 g IV every eight hours) should be used
instead of ceftriaxone or cefotaxime if Pseudomonas is
possible.
62. Duration of therapy
The duration of antibiotics for brain abscess is
prolonged, usually four to eight weeks.
This recommendation derives from retrospective
reports and reviews since no clinical trials have been
performed.
United Kingdom guidelines recommend four to six
weeks if the abscess has been drained or excised and
63. Surgery
The neurosurgeon needs to be contacted at the time
of initial diagnosis of a brain abscess.
Needle aspiration and surgical excision have both
used to treat brain abscess and are also required for
diagnosis, prior to the initiation of antibiotic therapy if
possible.
An exception may be when a brain abscess occurs in
the setting of bacteremia, in which case antibiotic
therapy is based upon the results of blood culture.
64. Aspiration
Needle aspiration is generally preferable to
surgical excision since the neurologic sequelae
are reduced.
Needle aspiration is preferred for speech
and regions of the sensory or motor cortex
in comatose patients
A Burr hole is placed and then needle
65. Surgical excision
Surgical excision is a more radical approach that
generally results in greater neurologic deficits and now
is infrequently performed.
However, excision may be the initial treatment of choice
in the following circumstances:
Traumatic brain abscesses (to remove bone chips
foreign material)
Encapsulated fungal brain abscesses
Multiloculated abscesses
66. In addition, the following are indications for
excision after initial aspiration and drainage:
No clinical improvement within one week
Depressed sensorium
Signs of increased intracranial pressure
Progressive increase in the diameter of the
68. ETIOLOGY
Neurocysticercosis is caused by the larval
form of Taenia solium (cysticerci).
is the most frequent helminthic infection of
the central nervous system.
Humans are the definitive hosts for this
parasite, and swine are the intermediate hosts.
69. Epidemiology
Approximately 2.5 million people worldwide
carry adult T. solium (Burneo and Garcı´a, 2001).
Conservative figures mention 50 000 deaths
every year due to NCC and no less than 20
million people infected with cysticerci of T.
solium.
Globally, NCC is considered to be the most
common parasitic disease of the nervous
system (Burneo and Garcı´a, 2001).
70.
71.
72. PATHOGENESIS
The adult tapeworm develops in human hosts
after they ingest live cysticerci in undercooked
pork.
Cysticercosis may develop in both humans
and swine that ingest food contaminated with
the feces of human carriers of adult cestodes.
Adult tapeworms shed proglottids that each
73. Neurocysticercosis with giant cysts has
generally been defined by the presence of a
cyst more than 50 mm in diameter.
Clinical manifestations that suggest an
expansile mass and intracranial hypertension.
Perilesional cerebral edema is also reported.
74. CLINICAL FEATURES
The most common manifestation of
neurocysticercosis is new-onset partial seizures.
Cysticerci may develop in the brain parenchyma focal
neurologic deficits.
When present in the subarachnoid or ventricular
spaces, cysticerci can produce increased ICP by
interference with CSF flow.
Spinal cysticerci can mimic the presentation of
intraspinal tumors.
75. When the cysticerci first lodge in the brain,
they frequently cause little in the way of an
inflammatory response.
As the cysticercal cyst degenerates, it elicits an
inflammatory response that may present
clinically as a seizure.
Eventually the cyst dies, a process that may
take several years and is typically associated
with resolution of the inflammatory response
and, often, abatement of seizures.
76. DIAGNOSIS
The lesions of neurocysticercosis are readily visualized by
MRI or CT scans.
Lesions with viable parasites appear as cystic lesions.
Lesions may appear as contrastenhancing lesions
surrounded by edema.
A very early sign of cyst death is hypointensity of the
vesicular fluid on T2-weighted images when compared
with CSF.
Parenchymal brain calcifications are the most common
77. MRI of parenchymal neurocysticercosis. ( a ) Viable cysts showing the scolex. ( b ) Colloidal cyst
appearing as a ring-enhancing lesion with perilesional edema
78.
79. The presence of antibodies
against T. solium in serum was
determined by Western blot
analysis in all patients.
80. TREATMENT
Intravenous dexamethasone every 8 hour
albendazole at a dose of 15 mg per kilogram of body
weight per day, administered in three divided doses, for
four weeks.
Praziquantel 100 mg per kilogram per day, in two divided
doses administered two hours apart,
Hydrocephalus developed were admitted to the hospital
and treated with a ventriculoperitoneal shunt before the
initiation of cesticidal treatment.
Neurosurgery may be required only when there is an
81. Reference
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• Tunkel, A. R., Glaser, C. A., Bloch, K. C., Sejvar, J. J., Marra, C. M., Roos,
K. L., … Whitley, R. J. (2008). The Management of Encephalitis :
Clinical Practice Guidelines by the Infectious Diseases Society of
America. 07740. https://doi.org/10.1086/589747
• Disclosures, C. (2019b). Viral encephalitis in adults.
• Venkatesan, A., & Geocadin, R. G. (2014). Diagnosis and management
of acute encephalitis: A practical approach.
https://doi.org/10.1212/CPJ.0000000000000036
• Especialidades, H. De. (2001). M E D I C A L T R E AT M E N T F O R N E U R
O CYST I C E R C O S I S C H A R AC T E R I Z E D BY G I A N T S U BA R AC
H N O I D CYST S MEDICAL TREATMENT FOR NEUROCYSTICERCOSIS
CHARACTERIZED BY GIANT SUBARACHNOID CYSTS. 345(12), 879–885.
• Granerod, J., & Crowcroft, N. S. (2007). The epidemiology of acute encephalitis.
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https://doi.org/10.1080/09602010600989620
Editor's Notes
VIRAL VERSUS POSTINFECTIOUS ENCEPHALITIS
Atypical presentations of rabies include seizures, cranial nerve palsies, and myoclonus.
however, the absence of rash does not eliminate VZV from consideration.
should always be initiated as soon as possible if the patient has encephalitis without apparent explanation.
This complaint is most commonly associated with occipital lobe abscess or an abscess that has leaked into a lateral ventricle
Grand mal seizures are particularly common in frontal abscesses., fever is not a reliable indicator