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Neuro 3…. Meningitis.. . Encephalitis. Trigeminal Neuralgia. Meningitis. Meningeal inflammation ...around brain and spinal cord. Cause: Viral vs Bacterial vs other…. Classic sx: HA, NV, neck stiffness, fever. epidemiology. WHO:infants <1yr & children 5 -10yr WHEN:

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Neuro 3 l.jpg

Neuro 3…

Meningitis..

Encephalitis

Trigeminal Neuralgia


Meningitis l.jpg

Meningitis

Meningeal inflammation

...around brain and spinal cord

Cause: Viral vs Bacterial vs other…..

Classic sx: HA, NV, neck stiffness, fever


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epidemiology

WHO:infants <1yr &

children 5 -10yr

WHEN:

highest incidence: late Spring to Fall

reflecting peak activity of enteroviral and arthropod-borne infections

Viral Meningitis: definition

Viral (Aseptic) Meningitis:

Meningeal inflammation w/ neg. bacterial cultures w/

No associated neurologic dysfunction


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VIRAL MENINGITIS: PATHOGENESIS

Few viral particles replicate in the nasopharynx with spread/replication in resp. tract lymphatics.

Most viral particles bind to specific receptors on enterocytes & traverse the intestinal lining cells to reach the Peyer's patches in the lamina propia, where they replicate on mucosal surfaces of the respiratory & GI tract

  • -->primary viremia (onset of illness) seeding of other organs (liver/spleen/heart)

  • second viremia(seedingof the CNS during first or second viremia)

  • s/sx of infx


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Viral meningitis: Causes

  • OTHER CAUSES

  • Mycobacteria

  • Fungi

  • Spirochetes

  • parameningeal infections

  • Medications

  • (Amox,. Bactrim, NSAIDS, zantac)

  • malignancy

MOST COMMON:

*Enterovirus (esp.Spring/Fall)

Coxsackie

Echovirus

other non-poliovirus enteroviruses

?arbovirus

  • OTHER VIRUSES

  • HSVHIVWest Nile virus (WNV)

  • varicella-zoster virus (VZV) Mumps

  • lymphocytic choriomeningitis virus (LCM)


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Most common cause: Enteroviruses

EV: 85 -95 % viral meningitis

Nonpolio-EV serotypes cycle from year to year

however, certain serotypes have remained prevalent.

Most common 2000-2005: Coxsackieviruses A9, B5, and B1

Echoviruses 6, 9, 13, 18, and 30

<3mo: usually group B coxsackie viruses and parecho viruses

EV 71, closely related to coxsackie virus A16, the viral agent of hand-foot-mouth disease, has emerged as a significant cause of aseptic meningitis, encephalitis, myelitis.

TRANSMISSION

Humans: only known reservoir

Transmission: fecal-oral route. (Rare:droplet inhalation)

Possible Transplacental -> stillbirth, abortion, neonatal infx


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Risk factors for EV

Seasonality

In temperate climates: most EV infections outbreak during the warmest months; however, sporadic cases can develop throughout the year.

In US: infections more frequent June - October

In tropical and subtropical regions: consistent thru year

  • Host factors:

  • severe nonpolio EV infx if immunodeficient, age extremes

  • risk of chronic meningoencephalitis if child w/ deficient humoral immunodeficiency, especially X-linked agammaglobulinemia

Incubation period for EV infection is approx. 3-6d


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Other viruses…Herpes viruses

  • All members of the Herpes viridae family can cause aseptic meningitis

  • USUALLY: HSV

  • INFREQUENTLY: CMV, VZV, human herpesvirus (HHV)-6, and Epstein-Barr virus (EBV)

  • Neonatal & CNSinfxs are the most devastating

  • Primary infection is followed by lifelong infection, w/ potential for reactivation

  • Humans are the only reservoir for transmission

  • Infections occur worldwide without seasonal prevalence

  • ? mechanisms of spread to the brain include: hematogenous dissemination, direct extension nasopharyngeal mucosa, or via neurogenic pathways


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VZV

  • Aseptic meningitis is a rare complication of chickenpox and herpes zoster

  • The syndrome known as zoster sine herpete is characterized by:

  • CSF pleocytosis

  • documented CNS infection with VZV by PCR

  • absence of typical skin lesions

**Decreasedincidence since introduction of varicella vaccine

CMV and EBV

RARELY CAUSE Aseptic Meningitis

however, aseptic meningitis is the most common neurologic complication seen in patients with primary EBV infection


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OTHER CAUSES: HHV-6 and HHV-7

  • HHV-6, (roseola or exanthem subitum)

  • common cause of febrile sz & meningitis in infancy

  • HHV-7, (also exanthem subitum)

  • causes febrile seizures in infancy

  • causes meningitis in children


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Other causes: Arboviruses

Highest incidence;: tropical, developing regions

US: most common after EV

The incubation period: 1 - 18 days

Most important endemic US arboviruses :

St. Louis encephalitis virus

West Nile virus

Eastern equine encephalitis virus

Western equine encephalitis virus

California encephalitis viruses

Pathogenesis : Viruses are inoculated subcutaneously or intravenously per vecotor (mosquito) bite

Replication in the skin or muscle

-> primary viremia

-> spreads to to the reticuloendothelial system or CNS.


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HISTORY..ask about exposure

Ask about symptoms

?rodents (LCM) ?ticks (Lyme) ?mosquitos

?human contacts

?TB ?sexual activity (HSV-2, HIV, syphilis)

Nonspecific sx:

Fever HA

Nausea & vomitingPhotophobia

Nuchal rigidityAltered mental status

(Kernigs/Brudzinski’s usu. neg)


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MENINGEAL IRRITATION

Physical Exam….look for


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PE:

Signs of meningeal irritation


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PE: Examination for nuchal rigidity

  • Passive or active neck flexion: inability to touch the chin to chest

  • lateral motion less reliable finding

  • Kernig's & Brudzinski's signs were originally developed and tested in patients with severe, late stage meningitis

  • Brudzinski's sign: spontaneous flexion of the hips during attempted passive flexion of the neck.

  • Kernig's sign: inability or reluctance to allow full extension of the knee when the hip is flexed 90º.

  • When LP was performed w/ suspected meningitis :

  • sensitivity extremely low (5% for each sign; 30% for nuchal rigidity)

  • specificity :95% for each sign & 68% for nuchal rigidity.

  • Jolt accentuation of headache more sensitive for dx meningitis.

  • Sensitivity: 97 % & specificity of 60 % for dx of CSF pleocytosis


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PE.. look for rash

DX: CSF

  • Diffuse maculopapular exanthem in mildly ill pt:

  • ?enteroviral infection, primary HIV, or syphilis. ?meningococcal infection & RMSF

  • Parotitis: mumps meningitis in unvaccinated pt.

  • Severe vesicular, ulcerative genital lesions: HSV-2

  • Oral thrush & cervical lymphadenopathy: HIV

  • Asymmetric flaccid paralysis: West Nile Virus


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csf


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TREATMENT: Suspectedviral meningitis

TREATMENT: if unclear etiology

Usually self-limited (vs bact.meningitis)

Resolves without specific therapy

  • Consider empiric therapy x 48hrs if Elderly, prior antibiotics, immunocompromised

  • Otherwise, consider observation

  • If suspect HIV: check HIV RNA and HIV antibody

  • If suspect HSV: acyclovir10 mg/kg IV q8hr

  • empiric antibiotics after blood / CSF cultures

  • OR observation with repeat LP in 6 - 24 hrs.

  • If symptomatically improved and culture negative: DC antibiotics w/o repeat LP

  • If persistent SX w/o clear dx: repeat LP


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HOSPITALIZE IF..

  • Ill-appearance

  • Signs of encephalitis

    • altered mental status, behavior, or personality

    • motor or sensory deficits

    • speech or movement disorders; hemiparesis; flaccid paralysis; paresthesias;

    • seizures

  • Need for empiric antimicrobial therapy.

  • Need for IV hydration or aggressive pain control.

  • Immunocompromised host.

  • Age younger than one year.


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Bacterial Meningitis“purulent meningitis”

  • Meningitis is an inflammatory disease of the lepto-meninges, the tissues surrounding the brain and spinal cord, and is defined by an abnormal number of WBCs in CSF .

  • Meninges:

  • pia

  • arachnoid

  • dura maters

  • Bacterial meningitis: infx of arachnoid mater and CSF in both the subarachnoid space and cerebral ventricles.


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Bacterial Meningitis - Causes

There are at least 50 causative bacteria

Community Acquired:

  • Streptococcus pneumo (pneumococcus)

  • Neisseria meningitidis (meningococcus)

  • Listeria monocytogenes (50-60ys, immunideficient)

  • Haemophilus influenzae type b (Hib)

  • Healthcare-associated

  • (after neurosurgery, ventricular drains, w/trauma )

  • usually staphylococci

  • aerobic gram-negative bacilli


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Symptoms

Quite ill

Rapid onset

Classic Triad:

*Fever (>38*) (95%x 4d)

*Mental status changes (78%)

*Nuchal rigidity (88% x7d)

Also:

Severe, generalized headache

Photophobia

Nausea/vomiting

Rash 11-26% N. meningitidis, petechiae and palpable purpura

Arthritis: 7% N. meningitidis,

PHOTO


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Additional Symptoms

Decreased consciousness

Rapid breathing

Agitation

Opisthotonos

Bulging fontanelles

Poor feeding

Irritability

NEWBORN FUO


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Possible Complications

Hearing loss

Brain damage

Loss of vision

Hydrocephalus

Waterhouse-Friderichsen syndrome (WFS) or hemorrhagic adrenalitis (Neisseria meningitidis )


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Differentials

Viral meningitis

Encephalitis

Febrile viral syndromes

Drug induced meningitis


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BACT. MENINGITIS :DX Tests

LP

Blood cx positive

Other lab:CBC, chem

Chest x-ray

(r/o other sites of infx)

Head CT scan (ICP )

(r/o hydrocephalus, abscess or deep swelling)

CSF glucose:

-<40 mg/dL or <1/2 serum

CSF CELL count:

- WBC’s >1000/microL with a predominance of neutrophils

PROTEIN elevated >0.4g/dl

POSITIVE gram stain/culture

H. Influenzae b Gram Stain

REFER!


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LABORATORY FEATURES

FYI

Routine blood work is often unrevealing.

WBC: usually elevated, with left shift

Leukopenia: possible w/ severe infection

Platelet count: may be reduced.

Leukopenia and thrombocytopenia = poor outcome

Coagulation studies: may have DIC.

Serum chemistry: may have metabolic acidosis or hyponatremia

Blood cultures often positive (50- 90%)

Obtain Two sets of blood cultures prior to the initiation of antimicrobial therapy

Cultures obtained after antimicrobial therapy are much less likely to be positive, esp. meningococcus

Tests of urine, mucosal surfaces for bacterial antigens are not generally helpful


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LUMBAR PUNCTURE

FYI

  • Every patient w/suspected meningitis should have CSF obtained unless LP contraindicated.

  • PROs of CT then LP:

  • exclude a mass lesion or increased ICP, which rarely leads to cerebral herniation during LP

  • However, a screening CT scan is not usually necessary

  • Study: CT:24%had abnl finding, but only 5% had mass effect.

  • Abnl CT scan predicted by a suspicious hx/Exam :

  • -immunosuppression

  • -previous CNS disease

    • seizure within the previous week

    • reduced LOC

    • motor or cranial abnormalities, papilledema

  • CONS of CT then LP:2hr delay in dx, 1hr delay in rx.


  • If lp is delayed l.jpg

    If LP is delayed…

    fyi

    Obtain blood cultures

    Start antibiotics empirically before the imaging study

    Also give dexamethasone (0.15mg/kg IV q6hr)

    shortly before or at the same time as the antibiotics

    ( rate of hearing loss & other neuro complications, & mortality)

    (Adjunctive dexamethasone should not be given after antimicrobial therapy b/c unlikely to improve pt outcome)

    Prior administration of antimicrobials tends to have

    minimal effects on the chemistry and cytology findings,

    but can reduce the yield of Gram stain and culture .

    However, a pathogen can still be cultured from the CSF in most patients up to several hours after the administration of antibiotics


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    TREATMENT

    Antibiotics - depending on organism

    Extremes of age (<3m or >60 yrs)

    cover for listeria with ampicillin.

    Empiric therapy : rocephin (2grams Q12h) plus vancomycin

    Treatment of secondary symptoms including cerebral edema, shock, sz

    FYI

    • TRUE medical emergency

    • requires immediate admission

    Any form of bacterial meningitis that is untreated or treated very late in its course is almost uniformly fatal.

    Sequelae

    In-hospital mortality 27%

    Neurologic deficit at discharge 9 %

    independent predictors of adverse outcome:

    hypotension

    altered mental status

    seizures

    ADVERSE OUTCOME:

    no RF — 9 %

    1 RF— 33 %

    2-3 RF — 56 %


    Antibiotics l.jpg

    Antibiotics

    FYI

    B/C uncertain effect of dexamethasone on the CSF penetration of vancomycin:

    Begin with vancomycin plus either ceftriaxone or cefotaxime.

    If susceptibility studies show intermediate susceptibility (MIC ≥2 mcg/mL) to ceftriaxone and cefotaxime, addrifampin

    B/C: vancomycin penetration into the CSF starts at a high level in the presence of bacterial meningitis..

    impairment in penetration to a level that will reduce efficacy is not likely in the first few days before susceptibility studies are available.


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    Patient Education

    Seek immediate medical attention if a child has any of the symptoms

    Early treatment is key to good outcome.

    Prevention of hflu: HiB vaccine

    Prevention of pneumococcal: Prevnar

    Prevention, high school students: Menactra

    Prophylaxis of household

    contacts w/ preventative antibiotics;

    highly recommended.


    Meningitis bacterial vs viral vs encephalitis l.jpg

    Meningitis (bacterial vs viral) vs Encephalitis

    Bacterial Meningitis

    Very serious

    Meningeal irritation

    CSF Gram stain positive

    CSF WBC >1000/microL (neuts)

    CSF glucose <40 mg/dL

    Nl brain

    function

    • Viral Meningitis:

    • less severe

    • meningeal irritation

    • fever, HA, NV

    • seizures

    • hemiparesis

    • flaccid paralysis

    • paresthesias

    • resolves w/o specific Rx

    • CSF WBC<500/ microL

    • CSF protein <80 100mg/dL

    • CSF glucose: normal

    • Gram stain negative

    Encephalitis

    Viral, invades brain tissue

    altered mental status (confused.. obtunded)

    motor or sensory deficits (paresis,  DTRs)

    altered behavior & personality speech or movement d/o

    No meningeal irritation

    Abnl brain function:


    Encephalitis l.jpg

    Encephalitis

    Viral Inflammation of the brain

    Rare disease

    (0.5 per 100,000)

    Most common in

    children

    elderly

    Immuno-compromised


    Encephalitis pathogenesis l.jpg

    Encephalitis: PATHOGENESIS

    • Two viral mechanisms:

    • 1.directly invade brain tissue (acute viral encephalitis)

    • virus cultured from the brain

    • viremia from viral meningitis

    • spread from peripheral nerves (rabies, HSV)

    • 2.Post-infectious encephalitis (autoimmune response)

    • No virus detected

    • hx of illness or vaccination 2-4wk prior to S/S

    • Need neuroimaging to differentiate.


    Encephalitis s s l.jpg

    Encephalitis…S/S

    subtle to profound…

    • Altered mental status: confused, agitated, obtunded

    • Behavior

    • Personality

    • Speech

    • movement.. Motor or sensory deficits : hemiparesis, cranial nerve palsies, exaggerated DTRs

    • Seizures are common

    NO S/S of meningeal irritation: photophobia, nuchal rigidity

    VS aseptic meningitis nonspecific, fever, headache, nausea, vomiting, photophobia, nuchal rigidity; nl cerebral function


    Neonates and young infants l.jpg

    Neonates and young infants

    As with other infections in neonates (0-28d) and young infants, the presentation can be nonspecific.

    • Fever (variable )

    • seizure

    • poor feeding

    • Irritability

    • Lethargy

    • In a series of 63 neonates with HSV1 CNS dz:

    • 49% lethargy

    • 57% seizure

    • 63% skin vesicles

    • 44% fever


    Children and adolescents l.jpg

    Children and adolescents

    SS at admission

    prospective series of 50 children (6wks-18yrs):

    100%:Encephalopathy 80%: Fever

    78% Seizure

    56% Other Focal

    neuro signs

    47%  LOC

    Complications

    status epilepticus

    cerebral edema

    inappropriate ADH

    cardiorespiratory failure

    DIC

    defined as depressed or altered LOC (lethargy, extreme irritability, significant change in personality or behavior) x ≥24hr


    Encephalitis causes l.jpg

    Encephalitis - Causes

    measles

    Many different viruses

    Most cause meningitis or encephalitis

    Postinfectiousencephalitis: MMR, VZV, influenza

    Sporadicencephalitis:HSV1

    Geographic location (eg, St. Louis encephalitis in North America, Japanese encephalitis in Asia)

    rmsf

    lyme

    • Tick Exposure:

    • Colorado tick fever (w. US) or

    • non-viral, ie: Lyme dz or RMSF


    Encephalitis causes40 l.jpg

    Encephalitis-Causes

    Mosquito exposure:

    • Arboviruses (east.equine, west. equine, St. Louis (NA, Midwest/So.US)

    • Venezuelan equine encephalitis

    2009

    • WNV (multiple continents including Asia, Africa, Europe, NA)

    • weakness, rash

    • rare < 1999,now most commonly CNS arboviral infx

    16


    Peds causes l.jpg

    Peds..causes

    *Enteroviruses—major cause.

    clear seasonality (78 % June - October)

    *HSV 1/11..5% all age groups but 75% neonatal infection

    Epstein-Barr virus—10 %

    Arbovirus La Crosse encephalitis: most common arbovirus in children

    Seasonal (July - September)usu 5-9yr\o

    Arbovirus West Nile virus .. rare

    Influenza virus:5 % usually< 5yo

    Other viruses MMR: rare b/c vaccinations


    Physical examination l.jpg

    physical examination

    IF Parotitis/mental status changes:Mumps encephalitis

    IF Flaccid paralysis: WNV infection

    Misdiagnosed as Guillain-Barre syn.

    Maculopapular rash 50%

    IF Tremors of eyelids, tongue, lips, extremities:

    St. Louis encephalitis or WN encephalitis

    IF Hydrophobia, aerophobia, pharyngeal spasms, hyperactivity: encephalitic rabies.

    Atypical : seizures, cranial nerve palsies, myoclonus

    IF Grouped vesicles in a dermatomal pattern: varicella-zoster virus


    Encephalitis differentials l.jpg

    Encephalitis - Differentials

    fyi

    noninfectious etiologies :

    intracranial tumors

    collagen vascular disorders

    vasculitis

    neoplastic diseases

    adverse effects of medications

    Other non-viral infectious etiologies

    Brain abscess

    Syphilis

    tuberculous meningitis

    fungal meningitis (eg, coccidioides

    REFER!!


    Encephalitis diagnostics l.jpg

    Encephalitis - Diagnostics

    Lumbar puncture:

    Serology test to detect the presence of antibodies

    EEG

    Brain imaging

    • Color: Clear

    • high pressure

    • WBC, usually < 250/mm3.

    • predominance of lymphocytes:

    • early infection -> Ý neuts

    • repeat @ 8 hr: shift to lymphs

    • protein < 150 mg/dL.

    • glucose nl (>50% of blood)

    • red cells : 0

    • (presence suggests HSV-1 )


    Diagnosis l.jpg

    DIAGNOSIS

    FYI

    Etiology in most cases remains undefined

    CSF:

    VS bacterial meningitis:

    higher WBC (>2000/mm3) w/ neuts predominantly

    higher protein concentration (>200 mg/dL) usually hypoglycorrhachia

    Culture— Viral culture of CSF routinely ordered but viruses recovered 6%

    polymerase chain reaction (PCR) tests for viruses

    PCR testing has replaced viral culture of CSF For HSV-1, HSV-2, and enteroviruses

    Most important viral etiology to r/o is HSV

    usually fatal if untreated


    Imaging l.jpg

    Imaging

    fyi

    CT/MRI : may or may be abnormal

    CT: r/o space-occupying lesions or brain abscess.

    MRI:detects demyelination


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    EMPIRIC THERAPY

    no specific therapies for most CNS viral infections.

    EXCEPT:

    HSV-1 / VZV :Acyclovir (10 mg/kg IV Q8h) initiated as soon as possible


    Prognosis l.jpg

    Prognosis

    IF diffuse cerebral edema or intractable seizures: poor neurologic recovery and increased risk of mortality

    IF self-limited seizure activity: rapid recovery

    IF HSV encephalitis :Even with prompt initiation of acyclovir, significant morbidity and mortality.

    one-year mortality:14 %

    epilepsy 24%

    neuropsychiatric sequelae 22 %


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    Encephalitis – Pt Education

    Mosquito avoidance!

    Avoid being outside at dawn and dusk (when mosquitoes are most active)

    Wear protective clothing

    Use insect repellent

    Drain standing water (breeding grounds for mosquitoes)

    Vaccinate Animal against rabies

    Acute phase lasts up to one week

    Full recovery can take several wks - months


    Trigeminal neuralgia l.jpg

    An extremely painful

    inflammation of the

    largest nerve in the

    skull: Trigeminal Nerve

    Trigeminal Neuralgia

    SX:

    Sudden, severe spasms

    usually unilateral

    Brief 1-3 sec

    stabbing or lancinating

    recurrent episodes

    Facial muscle spasms

    continuous dull pain b/t

    no nite awakening

    … pain in the distribution of one or more branches of the fifth cranial (trigeminal) nerve


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    Distribution of Pain

    • Distribution of pain usually V2 and/or V3 subdivisions of the trigeminal nerve (5CN)

    • V1 subdivision is involved in <5 % of pt

    • (V1 common in postherpetic neuralgia)

    • Trigger zones in the distribution of the affected nerve may be present and are often located near the midline.

    • Lightly touching these zones often triggers an attack,

    • Pain is triggered by touch or sounds

    • Pain during chewing, eating, drinking, shaving, or brushing teeth

    Distribution of pain


    Anatomy l.jpg

    ANATOMY

    FYI detail

    The trigeminal nerve (5th NN) is the sensory supply to the face & the sensory & motor supply to muscles of mastication.

    It has three major divisions:

    Ophthalmic (V1)

    Maxillary (V2)

    Mandibular (V3)

    The nerve starts at the midlateral surface of the pons, and its sensory ganglion (gasserian ganglion) resides in Meckel's cave in the floor of the middle cranial fossa.


    Triggers of paroxysms l.jpg

    triggers of paroxysms

    Triggers:

    chewing

    talking

    brushing teeth

    cold air

    smiling

    grimacing

    dental procedures

    Course: variable

    Duration: wks - months,

    followed by pain-free intervals.

    Recurrence: common,

    some have continuous pain.

    Severity:varies

    "pretrigeminal neuralgia" :dull, continuous, aching pain in the jaw evolving eventually into TN.


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    EPIDEMIOLOGY

    One of the most frequently seen neuralgias in the elderly.

    • Annual incidence: 4 - 13 per 100,000

    • Approximately 15,000 new cases in US/yr

    • Increases gradually with age

    • Most idiopathic cases >50yr

    • May occur 20’s, 30’s, rarely children

    • M: F ratio =1:1.5

    So.. suspect TN if F >50yo w/ sudden, lancinating, spasmodic facial pain


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    ETIOLOGY

    Usually caused by compression of the trigeminal nerve root,

    usually w/i a few mm of entry into pons

    80-90%:Compression by an aberrant loop of an artery or vein

    Corrupt

    Slide!

    • OTHERS:

    • acoustic neuroma

    • Meningioma

    • epidermoid or other cyst

    • rarely a saccular aneurysm or AVM

    vascular compression = classicTN

    structural lesions = secondary TN

    Mechanism: nerve compression -> demyelination in a circumscribed area around the compression -> sx


    Diagnosis per ihs l.jpg

    DIAGNOSIS per IHS

    FYI

    Based on Sx: paroxysms of pain in trigeminal nerve pathway

    The International Headache Society (IHS) dx criteria:

    Paroxysmal attacks of pain

    lasting from a fraction of a second to 2”,

    affecting one or more divisions of the trigeminal nerve

    Pain has at least one of the following characteristics:

    Intense, sharp, superficial, or stabbing

    Precipitated from trigger areas or by trigger factors

    Attacks are stereotyped in the individual patient

    There is no clinically evident neurologic deficit

    Not attributed to another disorder


    Trigeminal neuralgia differentials l.jpg

    Trigeminal Neuralgia - Differentials

    Dental pain

    Sinusitis

    Parotitis

    Temporal arteritis

    HSV type I

    Cluster or migraine headaches

    Posterior fossa tumors

    TMJ pain


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    Neuroimaging

    REFER!!

    head CT or MRI:r/o structural lesion (tumor, demyelinating lesions -MS)

    high resolution MRI/MRA :identify vascular compression

    Consider MRI if:

    Patients with trigeminal sensory loss

    Patients with bilateral symptoms

    Young patients (under the age of 40)

    Routine brain imaging identified a only 2° cause of TN in 15%

    Insufficient evidence to support or refute the utility of MRI to identify neurovascular compression in classic TN.


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    Electrophysiologic tests

    FYI

    • Trigeminal reflex testing :probably useful for distinguishing classic TN from secondary TN

    • trigeminal evoked potentials: not useful for making this distinction

    • Trigeminal reflex tests includes

    • the blink reflex (obtained by recording from the orbicularis oculi muscles after electrical stimulation of the supraorbital nerve [V1])

    • the masseter inhibitory reflex (obtained after electrical stimulation of the infraorbital [V2] and mental [V3] nerves).

    • Responses are recorded by surface electrodes using standard electromyography equipment.

    • Normal in patients with classic TN.


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    TN Treatment

    Anticonvulsants -

    Most common:

    1carbamazepine (Tegretol)

    2 oxcarbazepine (Trileptal)

    4phenytoin (Dilantin)

    Other anticonvulsants:

    3 lamotrigine (Lamictal)

    4 gabapentin (Neurontin)

    Antispasticity Agents -

    3 baclofen

    Tricyclic Antidepressants -

    Amitriptiline(Elavil)

    FYI

    INITIAL

    REFRACTORY..

    Alcohol injection - temporary pain relief by numbing the affected areas of face

    Surgery - goal:

    • either to stop the blood vessel from compressing the trigeminal nerve,

    • or to damage the trigeminal nerve to keep it from malfunctioning.

    1 EFFECTIVE,

    2 PROBABLY EFFECTIVE,

    3 POSSIBLY EFFECTIVE

    4 UNCERTAIN EFFECTIVENESS


    Patient education61 l.jpg

    Patient Education

    Avoidance of triggers

    Coping with pain

    Medication side effects

    Lab monitoring re: blood dyscrasias

    The end


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