infectious disease of the cns presented by: joseph s. ferezy, d.c

Infectious Disease of the CNSInfectious Disease of the CNS

Presented By:

Joseph S. Ferezy, D.C.

Lumbar PunctureLumbar Puncture

Common Diagnostic Test Diagnostic (Spinal Tap)

– Subarachnoid space– Examine

Pressure Microorganisms (and culture) Proteins (myelin basic) Blood

Lumbar PunctureLumbar Puncture

Therapeutic– Epidural Steroid– Proceedure

at L3-4 Interspace at L4-5 Interspace (@ Iliac Crests)

Lumbar Puncture Lumbar Puncture ContraindicationsContraindications

Intracranial Mass & Increase Intracranial Pressure (ICP)\

Through Infected Area

Lumbar Puncture Lumbar Puncture Normal

– Clear, Colorless, No Clot– 70-200 Mm H2O Pressure– Cells 0-5/mm3 (Mononuclear)– Na+, K+, Cl, - PH 7.35 - 7.40– Glucose 45-80 Mg%– Protein 5-15 Mg% (Ventricles), 10-25 Mg% (Cisternal), 15-45%

(Lumbar) – Gamma Globulins: 5-12% of Total Protein– BUN 5-25 Mg%– Bilirubin 0– Amino Acids 20% of Blood Level

Lumbar PunctureLumbar Puncture ComplicationsComplications

Headache - Still Fairly Common - Decrease in ICP & Traction on Meninges

Backache - Usually Due to Bad Technique and Many Attempts Causing Muscle Spasms

Intracranial Subdural Hematoma – Traction and Rupture of Veins

Infection - Non Sterile Procedure Uncal Herniation - From Rapid Decrease in

Pressure Traumatic Tap – Lacerated Vessels & Bleeding

Acquired Immunodeficiency Acquired Immunodeficiency SyndromeSyndrome

AKA: AIDSThe result of an infection with the human

immunodeficiency virus (also called HIV).Virus attacks cells of the immune system,

nervous system, and other body systems.


AIDS can cause some serious nervous system problems. These problems can be one of the most challenging aspects of the disease.

HIV infects the nervous system directly. Other viruses, fungi, bacteria, or parasites take

advantage of your weakened immune system and infect the nervous system.


AIDS-related cancers develop. AIDS drugs cause side effects that affect or

damage nerves. Dementia is a common type of mental change

caused by the AIDS virus. – Early symptoms include slowed thinking, and

poor short-term memory and concentration. – May have changes in behavior and physical

coordination.


Lymphoma - cancer of the lymph tissue that can occur in the brain.

Toxoplasma - parasite found in cat feces and raw meat. It causes patches of tissue death in the brain.

Symptoms include headaches and seizures. Typically diagnosed with imaging and blood tests.

Sometimes a brain biopsy is needed. New imaging techniques may revolutionize.


The AIDS virus may also damage the spinal cord.

With cord damage symptoms include leg weakness and lose control of bladder or occasionally bowel.

Other nerves may be damaged, causing symptoms of weakness, numbness, tingling, and burning pain in the limbs.


CNS damaged nerve cells do not repair themselves.

Even if the AIDS virus is brought under control, the damage may be permanent.

Simpson, D. M. et. al. Ann Intern Med 1994;121:769-785Focal central nervous system lesions in AIDS

Focal central nervous system lesions in AIDS. Left. Brain computed tomographic scan in a patient with toxoplasmosis shows a ring-enhancing lesion with surrounding edema in the right basal ganglia that compresses the frontal horn of the lateral ventricle, with midline shift. Right. Brain computed tomographic scan in a patient with a primary central nervous system lymphoma shows a homogeneously contrast-enhancing lesion (arrow) with edema adjacent to the frontal horn of the right lateral ventricle.


The antiviral drugs used to treat HIV infection may help slow the development of dementia.

Antidementia drugs may be used with memory loss and confusion.

Infection with toxoplasmosis may be prevented by taking a combination of trimethoprim and sulfamethoxazole.


Infection with HIV predisposes to the development of neoplasms.

There are currently four AIDS-defining malignancies– Kaposi's sarcoma (formerly most common)– Non-Hodgkin lymphoma (NHL)– Primary CNS lymphoma (PCNSL)– Invasive cervical carcinoma. patients.


AIDS-related lymphoma is generally divided into three types.– Systemic NHL, PCNSL, and the primary

effusion ("body cavity") lymphomas.– These disorders are primarily encountered in

patients with more advanced HIV infection, with a CD4 count that is usually below 100/µL


PCNSL accounts for up to 15 percent of NHLs in HIV-infected patients compared to only 1 percent of NHLs in the general population.

The reported incidence of PCNSL in HIV-infected patients is 2 to 6 percent (at least 1000 times higher than in the general population) and has been as high as 10 percent in autopsy series.


The most common histology was diffuse large B cell lymphoma (immunoblastic variant).

Although CNS involvement also occurs in AIDS-related systemic lymphoma in the form of secondary spread of the tumor to the meninges, the disease is limited to the CNS in PCNSL.


PATHOGENESIS — A small number of circulating B cells enter the central nervous system, and may do so in increased numbers as HIV infection advances.

Epstein-Barr virus (EBV) establishes latent, life-long infection in over 95 percent of adults.


During the course of HIV infection, EBV-specific T cells progressively lose the capacity to produce Interferon-gamma in response to EBV peptides.

In addition, EBV-positive B lymphocytes occur more frequently in the CNS of HIV-infected individuals than in normal brains.

Lyme DiseaseLyme Disease

Lyme disease, or borreliosis, is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia.

Borrelia burgdorferi is the predominant cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii are implicated in most European cases.

Borrelia bacteria, the causative agent of bacteria, the causative agent of Lyme disease. Magnified 400 times.Lyme disease. Magnified 400 times.

Lyme DiseaseLyme DiseaseLyme disease is the most common tick-borne

disease in the Northern Hemisphere. Borrelia is transmitted to humans by the bite

of infected ticks belonging to certain species of the genus Ixodes (the hard-bodied 'hard ticks').

Early manifestations of infection may include fever, headache, fatigue, depression, and a characteristic skin rash called erythema migrans.

IxodesIxodes ('hard ticks') ('hard ticks')

Erythema Chronicum Migrans Erythema Chronicum Migrans (ECM)(ECM)

Lyme DiseaseLyme DiseaseLeft untreated, late manifestations involving

the joints, heart, and nervous system can occur.

In most cases, the infection and its symptoms are eliminated with antibiotics, especially if diagnosis and treatment occur early in the course of illness.

Late, delayed, or inadequate treatment can lead to late manifestations of Lyme disease which can be disabling and difficult to treat.

Lyme DiseaseLyme Disease Some Lyme disease patients who have completed

a course of antibiotic treatment continue to have symptoms such as severe fatigue, sleep disturbance, and cognitive difficulties.

Some groups have argued that "chronic" Lyme disease is responsible for a range of medically unexplained symptoms beyond the objectively recognized manifestations of late Lyme disease, and that additional, long-term antibiotic treatment is warranted in such cases.

Lyme DiseaseLyme Disease Of four randomized controlled trials of long-term

ceftriaxone and doxycycline treatment courses in patients with ongoing symptoms, two found no benefit, and two found inconsistent benefits and significant side effects and risks from further antibiotic treatment.

Most expert groups including the Infectious Diseases Society of America and the American Academy of Neurology have found that existing scientific evidence does not support a role for Borrelia nor ongoing antibiotic treatment in such cases.


Symptoms– Lyme disease can affect multiple body systems,

producing a range of potential symptoms. – Not all patients with Lyme disease will have all

symptoms, and many of the symptoms are not specific to Lyme disease but can occur in other diseases as well.


The incubation period from infection to the onset of symptoms is usually 1–2 weeks, but can be much shorter (days), or much longer (months to years).

Symptoms most often occur from May through September because the nymphal stage of the tick is responsible for most cases.


Asymptomatic infection exists but is found in less than 7% of infected individuals in the United States.

Asymptomatic infection may be much more common among those infected in Europe.

Stage 1 – Early localized Stage 1 – Early localized infectioninfection

ECM occurs at the site of the tick bite 3 to 32 days after being bitten.

The rash is red, and may be warm, but is generally painless.

Classically the bullseye is seen, however, the partial clearing is uncommon, and thus a true bullseye occurs in as few as 9% of cases.

Lyme DiseaseLyme DiseaseErythema migrans is thought to occur in

about 80% of infected patients. Patients can also experience flu-like

symptoms such as headache, muscle soreness, fever, and malaise.

Lyme disease can progress to later stages even in patients who do not develop a rash.

SStage 2 – Early tage 2 – Early disseminated infectiondisseminated infection

Within days to weeks after the onset of local infection, the borrelia bacteria may begin to spread through the bloodstream.

Erythema migrans may develop at sites across the body that bear no relation to the original tick bite.


Another skin condition, which is apparently absent in North American patients, is borrelial lymphocytoma, a purplish lump that develops on the ear lobe, nipple, or scrotum.

Other discrete symptoms include migrating pain in muscles, joint, and tendons, and heart palpitations and dizziness caused by changes in heartbeat.


Acute neurological problems, which appear in 15% of untreated patients, encompasses a spectrum of disorders.

Facial or Bell's palsyMeningitis, characterized by severe

headaches, neck stiffness, and sensitivity to light.


Radiculoneuritis causes shooting pains that may interfere with sleep and abnormal skin sensations.

Mild encephalitis may lead to memory loss, sleep disturbances, or changes in mood or affect.

In addition, simple altered mental status as the sole presenting symptom has been reported in early neuroborreliosis.

Stage 3 – Late persistent Stage 3 – Late persistent infectioninfection

After several months, untreated or inadequately treated patients may go on to develop severe and chronic symptoms affecting many organs of the body including the brain, nerves, eyes, joints and heart. A myriad of disabling symptoms can occur.

Chronic neurologic symptoms occur in up to 5% of untreated patients.


A polyneuropathy manifested primarily as shooting pains, numbness, and tingling in the hands or feet may develop.

A neurologic syndrome (Lyme encephalopathy) is associated with subtle cognitive problems such as difficulties with concentration and short term memory.

Such patients may also experience profound fatigue.


Other problems such as depression and fibromyalgia are no more common in people who have been infected with Lyme than in the general population.

Chronic encephalomyelitis, which may be progressive, may involve cognitive impairment, weakness in the legs, awkward gait, facial palsy, bladder problems, vertigo, and back pain.


In rare cases, frank psychosis has been attributed to chronic Lyme disease effects, including misdiagnoses of schizophrenia and bipolar disorder.

Panic attack and anxiety can occur.Delusional behavior accompanied by a

depersonalization or derealization syndrome previously associated with early stages of general paresis.


Lyme arthritis usually affects the knees.In a minority of patients arthritis can occur

in other joints, including the ankles, elbows, wrist, hips, and shoulders. Pain is often mild or moderate, usually with swelling at the involved joint. Baker's cysts may form and rupture. In some cases joint erosion occurs.

TransmissionTransmission

Hard-bodied ticks of the genus Ixodes are the primary vectors of Lyme disease.

Transmission is relatively rare, with only about 1% of recognized tick bites resulting in Lyme disease: this may be due to the fact that an infected tick has to be attached for at least a day for transmission to occur.


In North America, the black-legged tick or deer tick (Ixodes scapularis) has been identified as the key to the disease's spread on the east coast.

Only about 20% of people who become infected with Lyme disease by the deer tick can remember having been bitten, making early detection difficult in the absence of a rash.

TransmissionTransmission Tick bites are unnoticed because of the small

size in the nymphal stage, as well as tick secretions that prevent the host from feeling any itch or pain from the bite.

The lone star tick (Amblyomma americanum), found throughout the Southeastern United States as far west as Texas, is unlikely to transmit the disease, though it may be implicated in southern tick-associated rash illness, which resembles a mild form of Lyme disease.


On the West Coast, the primary vector is the western black-legged tick (Ixodes pacificus).

The tendency of this tick species to feed predominantly on host species that are resistant to Borrelia infection appears to diminish transmission of Lyme disease in the West.


While Lyme spirochetes have been found in insects other than ticks, reports of actual infectious transmission appear to be rare.

Sexual transmission has been anecdotally reported; Lyme spirochetes have been found in semen and breast milk, however transmission of the spirochete by these routes is not known to occur.


Congenital transmission of Lyme disease can occur from an infected mother to fetus through the placenta during pregnancy, however prompt antibiotic treatment appears to prevent fetal harm.

DiagnosisDiagnosis

Diagnosed clinically based on symptoms, objective physical findings (such as erythema migrans, facial palsy, or arthritis), a history of possible exposure to infected ticks, as well as serological tests.

When making a diagnosis of Lyme disease, health care providers should consider other diseases that may cause similar illness.

DiagnosisDiagnosis

Most but not all patients with Lyme disease will develop the characteristic bulls-eye rash, and many may not recall a tick bite.

The EM rash, which does not occur in all cases, is considered sufficient to establish a diagnosis of Lyme disease even when serologies are negative.

DiagnosisDiagnosis

Serological testing can be used to support a clinically suspected case but is not diagnostic.

Diagnosis of late-stage Lyme disease is often difficult because of the multi-faceted appearance which can mimic symptoms of many other diseases the new "great imitator.“

DiagnosisDiagnosis

Lyme disease may be misdiagnosed as multiple sclerosis, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome (CFS), lupus, or other autoimmune and neurodegenerative diseases.

Laboratory testingLaboratory testingSeveral forms of laboratory testing for Lyme

disease are available, some of which have not been adequately validated. Most recommended tests are blood tests that measure antibodies made in response to the infection.

These tests may be falsely negative in patients with early disease, but they are quite reliable for diagnosing later stages of disease.

Laboratory testingLaboratory testingThe serological laboratory tests most widely available

and employed are the Western blot and ELISA. CDC: the more sensitive ELISA is performed first, if

it is positive or equivocal, the more specific Western blot is run.

The reliability of testing in diagnosis remains controversial, however studies show the Western blot IgM has a specificity of 94–96% for patients with clinical symptoms of early Lyme disease.

Laboratory testingLaboratory testing

Western blot, ELISA and PCR can be performed by either blood test via venipuncture or cerebrospinal fluid (CSF) via lumbar puncture.

Though lumbar puncture is more definitive of diagnosis, antigen capture in the CSF is much more elusive; reportedly CSF yields positive results in only 10–30% of patients cultured.


Single photon emission computed tomography (SPECT) imaging has been used to look for cerebral hypoperfusion indicative of Lyme encephalitis in the patient.

In Lyme disease patients, cerebral hypoperfusion of frontal subcortical and cortical structures has been reported.


In about 70% of chronic Lyme disease patients with cognitive symptoms, brain SPECT scans typically reveal a pattern of global hypoperfusion in a heterogeneous distribution through the white matter.

This pattern is not specific for Lyme disease, and is also seen in (CNS) syndromes such as HIV encephalopathy, viral encephalopathy, chronic cocaine use, and vasculitides.

Laboratory testingLaboratory testingAbnormal MRI findings are seen in both

early and late Lyme disease.MRI scans may demonstrate white matter

lesions on T2-weighted images, similar to those seen in demyelinating or inflammatory disorders such as multiple sclerosis, systemic lupus erythematosus (SLE), or cerebrovascular disease.

Cerebral atrophy and brainstem neoplasm has been indicated with Lyme infection as well.

PreventionPrevention

Attached ticks should be removed promptly.Protective clothing includes a hat and long-

sleeved shirts and long pants that are tucked into socks or boots.

Light-colored clothing makes the tick more easily visible before it attaches itself.

People should use special care in handling and allowing outdoor pets inside homes because they can bring ticks into the house.

PreventionPrevention

A more effective, community wide method of preventing Lyme disease is to reduce the numbers of primary hosts on which the deer tick depends such as rodents, other small mammals, and deer.

Reduction of the deer population may over time help break the reproductive cycle of the deer ticks and their ability to flourish in suburban and rural areas.

VaccinationVaccinationA recombinant vaccine against Lyme disease

was developed by GlaxoSmithKline was approved by the FDA on December 21, 1998.

Subsequently, hundreds of vaccine recipients reported that they had developed autoimmune side effects.

Supported by some patient advocacy groups, a number of class-action lawsuits were filed against GlaxoSmithKline alleging that the vaccine had caused these health problems.

VaccinationVaccinationThese claims were investigated by the FDA

and the CDC, who found no connection between the vaccine and the autoimmune complaints.

Despite the lack of evidence that the complaints were caused by the vaccine, sales plummeted and LYMErix was withdrawn from the U.S. market by GlaxoSmithKline in February 2002 in the setting of negative media coverage and fears of vaccine side effects.

Tick removalTick removal

It is generally agreed that the most effective method is to pull it straight out with tweezers.

Data have demonstrated that prompt removal of an infected tick, within approximately 36 hours, reduces the risk of transmission to nearly zero; however the small size of the tick, especially in the nymph stage, may make detection difficult.

TreatmentTreatmentAntibiotics are the primary treatment for Lyme

disease; the most appropriate antibiotic treatment depends upon the patient and the stage of the disease.

The antibiotics of choice are doxycycline (in adults), amoxicillin (in children), and ceftriaxone.

In later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to treat.

TreatmentTreatment

Late diagnosed Lyme is treated with oral or IV antibiotics.

A very small minority of Lyme disease patients who have completed a course of antibiotic treatment, in the early stages of infection, continue to have symptoms such as severe fatigue, sleep disturbance, and cognitive difficulties.

TreatmentTreatmentWhile it is undisputed that these patients can have

severe symptoms, the cause of these symptoms and treatment of such patients is disputed.

Some attribute to persistent infection or coinfections.

“Chronic" Lyme disease has been cited as responsible for a range of medically unexplained symptoms beyond the objectively recognized manifestations of late Lyme disease, with or without any evidence of past or present infection.

TreatmentTreatmentStudies have shown little to no benefit from

30 days of IV antibiotics and 60 days of oral antibiotics with high placebo rates.

Debate rages regarding long term antibiotic treatment, but complications of the treatment are well documented.

TreatmentTreatment

The Infectious Diseases Society of America and the American Academy of Neurology, have concluded that there is no convincing evidence that Borrelia is implicated in the various syndromes of "chronic Lyme disease", and recommend against long-term antibiotic treatment as ineffective and possibly harmful.

TreatmentTreatmentIt is well established that there are

significant side effects and risks of prolonged antibiotic therapy, and at least one death has been reported from complications of a 27-month course of intravenous antibiotics for an unsubstantiated diagnosis of "chronic Lyme disease".

TreatmentTreatment

A number of other alternative therapies have been suggested, though clinical trials have not been conducted.

Hyperbaric oxygen therapy (which is used conventionally to treat a number of other conditions), as an adjunct to antibiotics for Lyme has been discussed.

Alternative MedicineAlternative Medicine

Approaches include bee venom because it contains the peptide melittin, which has been shown to exert inhibitory effects on Lyme bacteria in vitro.

PrognosisPrognosis

For early cases, prompt treatment is usually curative.

The severity and treatment of Lyme disease may be complicated due to late diagnosis, failure of antibiotic treatment, and simultaneous infection with other tick-borne diseases (co-infections) and immune suppression in the patient.

PrognosisPrognosis

Many patients with Lyme disease have fatigue, joint or muscle pain, and neurocognitive symptoms persisting for years despite any treatment.

Patients with late stage Lyme disease have been shown to experience a level of physical disability

In rare cases, Lyme disease can be fatal.

Bacterial InfectionsBacterial Infections

Acute Pyogenic (Bacterial) Meningitis– Organisms

Diplococcus Pneumoniae Neisseria Meningitidis Haemophilus Influenzae

– Metastasis Hematogenous Route Extension - Otitis Media, Scalp, Sinusitis Trauma – Open After Neurosurgery or Lumbar Puncture – Rarely

Acute Pyogenic (Bacterial) Acute Pyogenic (Bacterial) MeningitisMeningitis

Clinical– Children (6 Months - 1 Yr Greatest Risk) Under 15 Yr =

75% of All Cases - Usually in Winter Months – Usually Post Infection - Lungs, Ear, Sinus, Skull Bones,

Throat, Nasopharynx, Mastoids, Exposure to Meningococcus, Head Trauma, Neurosurgery, Spinal Anesthesia, Chronic Debilitation, Immunosuppression

– Signs Stiff & Painful Neck Positive Kernig & Brudzinski Tests High Fever Clouded Consciousness & Sensorium

Acute Pyogenic (Bacterial) Acute Pyogenic (Bacterial) MeningitisMeningitis

Course– May Be Quick (Poor Prognosis) or Insidious – Days to

Weeks (Better Prognosis)

Management - M.D. Referral– Complete Bed Rest– Fluid & Electrolyte Maintenance – Antibiotics– 10 - 20% Die (Especially the Very Young & Old)

Brain AbscessBrain Abscess

In Brain Parenchyma Usually Hematogenous Spread (Otitis Media,

Sinusitis, Ect.) Clinical

– 2:1 Male:female– Fever, Chills, H.A., Focal Neurological Signs– Symptoms of Intracranial Mass – Papilledema, Decreased Pulse & Respiration – M.D. Referral

Spinal Epidural Abscess (Acute)Spinal Epidural Abscess (Acute)

Usually Diabetic With Other Area of Infection or Minor Back Trauma or IV Drug Abuse

Usually After Other Infection Usually Begins As Osteomyelitis Clinical

– Spinal Pain– Radicular Pattern – Cord Compression – Paraparesis – Paraplegia – Loss of Bladder &/or Bowel Function– Increased Msr's + UMN Signs With Sensory Loss Below

Level of Lesion

TetanusTetanus

Neurotoxin of Clostridium Tetani Periodic, Severe Muscle Spasms Clinical

– Usually After a Deep Puncture Wound (Obligate Anerobe) With Infected Soil

– Can Be After Scratch, Insect Bite, Vaccination, or Without a Wound

– Incubation = 4 to 10 Days After Infection, Can Be Hours to Weeks

– Chills, Fever, Pain & Swelling at Site of Infection– Attacks Motor Neurons (Tetano-spasmin) = Lock Jaw

(Trismus) & Risus Sardonicus (Sardonic Smile)early

TetanusTetanus

More Muscles Become Involved Brief & Intense Spasm Increasing in Frequency –

More Powerful Muscle Groups Cause Characteristic Posture During Contractions

May Fracture Bones Diagnosed by Clinical Picture M.D. Referral Prognosis

– Quick Symptoms = Poor Prognosis – Death Early - Longer Survive = Better Prognosis

BotulismBotulism

Definition - Acute, Often Fatal Toxemia From Ingestion of Neurotoxin Causing a Descending Muscle Paresis & Paralysis

Etiology– Anerobe– Most Powerful Toxin Known to Man – Usually Improperly Home Canned Foods (Especially

Green Beans) – Interferes With Actylcholine & Peripheral Nerves

BotulismBotulism

Clinical– Usually Home Canned Green Beans (Look for Outward

Buckling of Can) – 12 to 36 Hours After Ingestion

Diplopia, Ptosis, Photophobia, Dysphagia, Dysphonia, Dysarthria, Descending Flaccid Paralysis May Paralyze Diaphragm

– Patient Is Alert, Afebrile, & No Sensory Loss– Refer to M.D.– Notify C.D.C. In Georgia (404)-329-3311

BotulismBotulism

Prognosis– Residual Paralysis (Ocular)– 50-70% Die

Brucellosis (Cerebral)Brucellosis (Cerebral)

Febrile With Associated FeaturesInfected Farm Animal Contact or Milk Refer to M.D. For Antibiotics Tetracycline)

PsittacosisPsittacosis

Infected Wild/domestic BirdsMeningitis or EncephalitisRefer to M.D. For Antibiotics

(Tetracycline)

Granulomatous InflammationsGranulomatous Inflammations Syphilis

– Meningitis - Usually Mild During 1st Stage, Severe in 2nd & 3rd Stage – Clinical - Acute Meningitis– Chronic Basal Meningitis– Usually With Tertiary Syphilis – Cranial Nerve Involvement III, VI and Eventually II– Syphilitic Arteritis– Panarteritis– TIA or Infarction Symptoms (Usually M.C.A.)– Syphilitic Gumma– Mass of Granulation Tissue (Rare in CNS)– Usually With Tertiary Syphilis

General ParesisGeneral Paresis

Chronic Syphilitic EncephalitisMental Status Deterioration, Tumor

Symptoms & Argyll- Robertson Pupils (Always!)

Syphilitic Optic Atrophy – Progressive– Restriction of Visual Fields – Total Blindness

Within Ten Years

Congenital NeurosyphilisCongenital Neurosyphilis

Fetus Infected @ 4th Month of Pregnancy

Spinal Cord SyphilisSpinal Cord Syphilis

Acute Transverse Myelitis – Tabes Dorsalis– Dorsal Nerve Roots & Posterior Columns (Usually

Tertiary)– Paroxysmal Lancinating Pains in Lower Limbs for Years

= (Lightening Pains)– Ataxia - Slapping Gait With Rombergs Sign– Paresthesias Common– Argyll-robertson Pupils– Charcot Joints (Due to Decreased Pain) – Bilateral Ptosis

Tuberculous MeningitisTuberculous Meningitis

Exposure Is Inhalation Hematogenous Spread Clinical

– Usually Been Overseas (Increased Mortality)– Hiistory of Contact With TB Patient– Anorexia, HA, Lethargy, Pain in Muscles, Nuchal

Rigidity – Meningitis & Increased ICP Signs – Spread From “Cold Abscess” of Chronic Spinal

Epidural Abscess

TuberculomaTuberculoma

In BrainSigns of Intracranial Mass (ICM)

SarcoidosisSarcoidosis

Unknown EtiologyClinical

– 20-40 Yrs.– Any Organ (Cns ~ 5%)– I.C.M. Signs

RickettsialRickettsial

TyphusRocky Mountain Spotted Fever (RMSF) Clinical

– RMS Fever Cases– Severe Encephalitis (Seizures, Neurological

Deficits)– Vomit, H.A., Fever, Maculopapular Rash on

Ankles & Wrist

Fungal InfectionsFungal Infections

Enter CNS Via Hematogenous or Directly Clinical

– Chronic Illness, Relapsing Fever – Predisposed

Antibiotic Therapy Immunosuppression Malignancy Debilitating Illness Trauma Endemic Area Prior History

Fungal Infections Fungal Infections

Signs & Symptoms– Headache– Anorexia– Vomiting– Insomnia– Meningeal Irritation– Papilledema– Focal Neurologic Signs– Hemiparesis– Other Organs Involved– Phycomyceles (Mucor Mycosis)

Fungal InfectionsFungal Infections

(Chronic Sinusitis Sudden Unilateral Blindness, Redish Black Nasal Discharge, 3,4,&/or 6th Cranial Nerve Involvement)

100% Fatal If UntreatedM.D. Refer

ProtozoanProtozoan Toxoplasmosis

– Asymptomatic– Brain Damage to Developing Fetus– Domestic & Other Animals– Ingest Cat Feces With Oocyst or Uncooked Meat With Encysted Trophozoites– Hematogenous– "Walled Off" by Body– Granuloma Calcify

Clinical– Asymptomatic– Predisposed

• Meningioencephalitis• Congenitally• Hepatosplenomegaly• Jaundice, Hydrocephalus, Encephalitis• Fatal or Brain Damaged

Amebiasis (CNS)Amebiasis (CNS)

Naegleria– Affects Child & Young Adults – Through Nasal Passages in Infected H2O (Lake or

Improperly Chlorinated Pools)– Acute, Fever, Nausea, HA, Stupor, Seizure, Coma ~

100% Fatal Malaria

– Rare in CNS– History of Malaria– Acute, Confusion, Clouded Consciousness, Stupor, &

Coma

CysticerosisCysticerosis

Definition - Larval Stage of Pork Tapeworm Ingested Eggs From Adult Worm Stomach to Body to Brain Cyst - Encapsulate - Calcify & Die Endemic in Mexico, SA, Asia, Southern US Usually Child & Young Adult Presents With Muscle Pain, HA, Nausea, Vomiting,

Seizures, Confusion, Delusion Subcutaneous Nodules & Muscle Tenderness Papilledema

Hydatid Disease Hydatid Disease (Echinococcosis)(Echinococcosis)

Larvae of Sheep Tapeworm in Body TissuePetting Infected Dogs – Food Ingest Entire

Body Usually a Child Ruptured Cyst in Muscle = Myositis - in

CNS = Severe ICM

ViralViral

Enteroviruses Usually Aseptic Meningitis (Summer & Fall)

Arthropod - Bore = Encephalitis Viral Meningitis

– Syndrome of HA, Meningeal Irritation Signs

Caused by Enterovirus or Mumps Virus (Winter & Spring)

Leptomeninges Leptomeninges

Most CommonClinical

– Usually Child & in Epidemics– Enterovirus in Summer & Fall, Mumps in

Winter & Spring– HA, Fever, Vomiting, Meningeal Irritation– Usual Full Recovery– Treat Symptoms

Viral EncephalitisViral Encephalitis

Acute, Febrile, Meningeal Irritation, HA, Vomiting

Blood Sucking Vectors (Mosquito or Tick) Herpes Encephalitis

– Type I, Acute, Frequently Fatal Encephalitis – Clinical

Child or Adult, Male &Female

Flu Like Symptoms (Fever, HA, Malaise) Meningeal Irritation, & Disorientation, Psychosis, Memory

Disturbances

Rhabdovirus (Rabies)Rhabdovirus (Rabies)

Acute, Often Fatal Clinical

– Usually Skunks (50%),– Bats (20%?)– Raccoons– Can Be Mother Nursing Baby, Infected Aerosol, Rabid

Donar to Corneal Transplant Recipient– History of Bite– Incubation of 1-2 Months– Pain & Paresthesias at Bite Site, With Fever, Chills, HA,

Myalgia

Rhabdovirus (Rabies) Rhabdovirus (Rabies)

"Furious" Rabies – Cyclic Breathing, Muscles Spasms on Attempted Swallowing

Terror at Thought of H2O = Hydrophobia Autonomic Disturbances Meningeal Irritation, Nerve Palsies If Bitten by Vampire (Bat) = Dumb or Paralytic

Rabies = Acute Ascending Paralysis

Reye Syndrome Reye Syndrome

Definition – Acute Encephalopathy Occurs Predominantly in Child

Follows Antecedent Viral Illness - Associated With Use of Aspirin (ASA)

Clinical– Acute Onset, Child Recovering From Flu,

Varicella, Upper Respiratory Infection

Reye Syndrome Reye Syndrome Stages

– Lethargy & Protracted Vomiting– Impaired Consciousness With Hallucinations, Combative Behavior &

Hyperventilation.– Coma With Intermittent Decerebrate Rigidity & Brainstem Reflexes

Intact– Coma With Decerebrate Rigidity– Coma, Respiritory Failure & Death – Liver Function Abnormal – Low Glucose– Serum Ammonia Abnormal – Occasionally Fatal –– Normal Recovery Usual - Rare Reoccurrence

Slow Viral InfectsSlow Viral Infects

Subacute Sclerosing Panencephalitis (SSPE)

Measles Virus?– Clinical Males:females 3:1– Onset 5 - 15 Years– Determined in School Personality, Speech

Problems, Papilledema– Myoclonus, Alexia, Spasticity

infectious disease of the cns presented by: joseph s. ferezy, d.c

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weakened immune system

cord damage symptoms

lumbar puncture normal