CASE REPORT

1
CASE REPORT

• ???? ????? ?"? ??????
• ????? ??????????
• ??" ????????? ?????

2

• ?? 67 , ???? 3, ????,
• ????? ,????? ???????
• ??? ????? ???, ??? ????? ?????? ????.
• ????? ????? ???? 20 ???

3
???? ??????

• ???? ???? 2005 ???? ???
• ??? ????????? ?? 38.5
• ????? ???????-????? ????? ??? ??? ????? ?????.
• ???? ?????, ???? ???? , ??? ???? ?????, ??? ????
  ???
• ???? ???"?- ??? ???? ???? ????- ????? ( ????)

4
????? ????? ( 28.08 )

• ??? ????????? ???? ???
• ????? ?????????? ??????? ?????( ??? ??????
  ???????????)
• ??????????? ???
• CRP- ????
• ????? ?? ?????
• ?????? ???????? ???????- ??????,
• ??????- ??????
• ??????? ( B, ,C A)- ?????
• CMV, EBV- ??? ???? ????? ?????
• ???????? ?? ???- ??? ?????????, ?????????- ??
  ???????.

5
????? ?????

• PPD- ?????
• CT ??? ????- ????
• CT ??- ????
• 7.09.05- ????? ???? ??? ????
• ????? ????? I (7.09.05)- ????? 130 , ???? 18,
  ????? ???? ?????????????
• HSV PCR - ?????, ????? INDIA- INK - ?????? ,
  ????? ???- ?????- ??????
• ????? CSF?????

6
????? ?????

• EEG - ????
• MRI ???
• ????? ?? ????? ????, ???????, ???? ???
  ?????????? ?????. ??????? ????? ????????? ????
  ????? ?????? ????? ????

7
????? ??????

• CHRONIC MENINGITIS
• WITH HYPOGLYCORRHACHIA
• LYMPHOCYTIC PLEOCYTOSIS
• PROTEINORRHACHIA
• ????? ???? ??????
• ????? ?????
• ??? ?
• TUBERCULOUS MENINGITIS

8
??? ?????? ???? ????????
9
CHRONIC MENINGITIS causes

• Infectious
• Tuberculosis and atypical mycobacterial
• Fungal cryptococcal, coccidial, histoplasmal,
  blastomyces etc.
• Nocardia
• HIV
• Herpes type 2( recurrent Mollaret meningitis)
• Lyme disease
• Syphilis
• Brucellosis
• Incompletely treated bacterial meningitis

10
CHRONIC MENINGITIS causes

• Granulomatous and vasculitic
• Sarcoidosis
• Wegener granulomatosis
• Bechet disease
• vasculitis

11
CHRONIC MENINGITIS causes

• Neoplastic
• Carcinomatous
• Lymphomatous
• Chemical
• Idiopathic
• Vogt-Kayanagi-Harada
• No cause determined in one-third of cases

12
CHRONIC MENINGITIS causes

• Tuberculosis- most common identifiable cause
• Smaller number neoplastic and cryptococcal
  meningitis
• Q j med 63283, 1987, Anderson NE

13
?? ??? ?????? ????? ???????? ????? ?????

• ????? ???? ????????? ?????? ???????? ?? ??? ????
  ???? ? CSF TB, NM,CRYP M
• ?? ??? ??????? ????? ????? ??? ??? ????? CSF
  ???? ???? ???? TUBERCULOUS CRYPTOCOCCAL
  NEOPLASTIC ??? ?????? ????? ???????? ?????????.

14
Tuberculosis

• 1/3 world population infected
• 8 million new cases each year
• 3 million deaths
• leading cause of death in HIV
• 95 of all cases in developing countries

15
Pathogenesis 5
natural history following TB exposure
What are the likely outcomes following exposure
to open TB?
16
TB MENINGITIS

• primary focus-- hematogenously spread -- subpial
  or subependymal cortical focus (ie, Rich
  focus)granuloma-- erodes into the subarachnoid
  space causing basal leptomeningitis
• Complications-hydrocephalus, vasculitis(
  involving the lenticulostriate and
  thalamoperforatoring arteries may occur and cause
  small infarcts in the deep gray nuclei and deep
  white matter)

17
TB MENINGTIS CT
18
Histology Preparation - Granuloma
19
VASCULITIS IN TB MENINGITIS

• Infarction is common (gt50 of patients) in the
  acute phase and results from a vasculitis that
  involves the pontine perforator,
  lenticulostriate, and thalamoperforator arteries.
  Small infarcts are common in the basal ganglia
  and brainstem.

20
VASCULITIS IN TB MENINGITIS
21
OTHERS COMPLICATIONS OF TB MENINGITIS

• Papilledema is the most common visual effect of
  TBM - secondary optic atrophy, other causes of
  visual impairment-chorioretinitis, optic
  neuritis, internuclear ophthalmoplegia and,
  occasionally, abrupt onset of painful
  ophthalmoplegia.
• Cranial nerve VI is affected most frequently by
  TBM, followed by III, IV, VII and, less commonly,
  CN II, VIII, X, XI, and XII (Zuger et al, 1997).
• Sudden onset of focal neurological deficits-
  vasculitis still appears to be the leading cause.
  
• Tremor is the most common movement disorder seen
  in the course of TBM. In a smaller percentage -
  choreoathetosis and hemiballismus(children gt
  adults)
• Myoclonus and cerebellar dysfunction .Deep
  vascular lesions are more common among patients
  with movement disorders

22
TB MENINGITIS

• TBM is more common in patients who are
  immunosuppressed, such as older persons, young
  children, patients with HIV, patients with
  diabetes, and patients taking steroids or
  cytotoxic drugs

23
CSF ? TB MENINGITIS

• ??? ????? ???? ?? ????, ????? ????- 80-400 ??"/
  ??, ???? ???? lt 40 ??" ?? , 200-400 ???? ?????
  ??????????
• ????? ?? ??????? TB ?? TUBERCULOMAS ?????? ?????
  ????? ?????? ?? CSF
• ???? ? 5 ???? ??? 11 ??????? ?? HIV ?????, 5
  ??????? ?? HIV ?????
• ?????? ????? ????? ????? ????? ????
  ????????????????? ?? ???????????? ? CSF

24
??? ???? ?????? ?? ?MENINGITIS TB

• ????? AFB ????? CSF -???? ?????? ? 10-30 ???????
  ????
• ????? CSF ???? ????? ????? ?? 6-8 ??????, ??????
  45-70
• PCR ? TB 70-75 ?????? false-negative ?????
  ???? ???? ???? ?? AFB ?????? ????-2 CFU ?? ????
  ???"
• PPD ????? ?? ? 50
• ????? AFB ? CSF ?? ???? ?? ?????? !!
• ????? CSF ?????? ?? ????? ?????!!!
• ?? ?????? ????? ?????? ?? ??? ????? ??????

25
Methods to increase mycobacterial yield of CSF
smear examination

• examine the deposit on centrifugation of a 10 ml
  CSF sample
• examine the deposit for at least 30 min
• examine several CSF samples over a few days
• Postgrad Med J 199975133-140  

26
Epidemiology 2
Microbiology (1)

• .

M. tuberculosis appearing as bright red bacilli
(rods) in a sputum smear stained with the
Ziehl-Neelsen stain
27
Epidemiology 3
Microbiology
Typical small, buff coloured colonies of M.
tuberculosis on Lowenstein Jensen medium
28
Diagnostic features of tuberculous meningitis

• Clinical
• fever and headache (for more than 14 days)
• vomiting
• altered sensorium or focal neurological deficit
• CSF
• pleocytosis (more than 20 cells, more than 60
  lymphocytes)
• increased proteins (more than 100 mg/dl)
• low sugar (less than 60 of corresponding blood
  sugar)
• India ink studies and microscopy for malignant
  cells should be negative
• Imaging
• exudates in basal cisterns or in sylvian fissure
  hydrocephalus
• infarcts (basal ganglionic)
• gyral enhancement
• tuberculoma formation
• Evidence of tuberculosis elsewhere
• Postgrad Med J 199975133-140  

29
Treatment

• Administration of a single antibiotic in the
  treatment of TB has been shown to lead to the
  development of mycobacteria resistant to that
  drug
• Combination chemotherapy is the treatment of
  choice effective regimens for the treatment of
  TB must contain multiple drugs to which the
  organisms are sensitive
• Using drug combinations minimises the development
  of drug-resistant strains

30
TREATMENT OF TB MENINGITIS

• First-line therapy -isoniazid, rifampin,
  pyrazinamide, streptomycin/ ethambutol.
• Second-line therapy - ethionamide, cycloserine,
  para-aminosalicylate (PAS), as well as
  aminoglycosides, capreomycin, and thiacetazone

31
TREATMENT OF TB MENINGITIS

• Adjunctive treatment with dexamethasone improves
  survival in patients over 14 years of age with
  tuberculous meningitis but probably does not
  prevent severe disability.
• N Engl J Med 2004, volume 351 1741-1751

32
Treatment of TB MENINGITIS

• The duration of conventional therapy is 6-9
  months, although some investigators still
  recommend as many as 24 months of therapy.

33
Treatment of TB MENINGITIS

• One recommended regimen for initial treatment of
  CNS TB is with isoniazid   (INH), RIF,
  pyrazinamide  , and ethambutol or streptomycin
  (SM). If there is satisfactory clinical
  improvement after 2 months, three- or four-drug
  regimens can be consolidated to two agents,
  usually INH and RIF, for an additional 10 months
• NICP, WALTER G. BRADLEY

34
staging of tuberculous meningitis

• Stage I prodromal phase with no definite
  neurological symptoms
• Stage II signs of meningeal irritation with
  slight or no clouding of sensorium and minor
  (cranial nerve palsies), or no neurological
  deficit
• Stage III severe clouding of sensorium,
  convulsions, focal neurological deficit and
  involuntary movements
• Postgrad Med J 199975133-140  

35
Worst prognostic factors for tuberculous
meningitis

• Most important
• Stage III (mortality 50-70)
• Others
• extreme of ages
• malnutrition
• presence of miliary disease
• presence of underlying debilitating disease, eg,
  alcoholism
• hydrocephalus
• focal neurological deficit
• low CSF glucose levels
• markedly elevated CSF protein
• Postgrad Med J 199975133-140  

36
TB MENINGITIS PROGNOSIS

• TB meningitis - life-threatening illness.
• Untreated, it is nearly always fatal, usually
  within 3-6 weeks of presentation.
• Even with treatment, a 21 mortality rate for
  immunocompetent patients and 33 for HIV-infected
  patients has been reported

37
????? ?????

• ???? ????? ??? ???? ???? 4 ??????
  IZONIAZID,PYRAZINAMIDE ETHAMBUTOL, RIFAMPIN
  ??????????
• ???? 3 ???? ??? ??? ??? ??? ???? ??????
• ????? ??? ??????

38
????? I ?????? II

• ???? ??????? ???? ????? ????-????? ?? 4 ??????
  ?????????? ?????? ?? 5 ??" ????
• ???? ????? ?????? ????? ?????? ?????-?????????
• ????? ??? -????? ?? ????? ????-?????
• ???? ?????? ?????? ???????- ????? ????? ?
  IZONIAZID ????? ????? ? 3 ?????? ????? ?? ???
  ??????? ( ???? ????????) ???? ???? ????? ?????
  ????? ? ETHAMBUTOL.

39
????? II

• ?????? ????? ????? CSF ?????- ??????
• ?????? ????-????? ?????
• ????? ???? ????? ????- ??? ?????? ???? ???, ???
  ?????????

40
??? ?????? ????? ???? ????? ????? ????? CSF
?????? !!!
41
????? ?????

• ??? 38.5, ???? ???
• ????? ?????( 21.12.05)- WBC 200, PMN 68, 34
  ????????????? , ????? 79, ???? 35.
• ????? ????? CSF
• ????? ???????, ????? ??????????

42
????? ?????

• ????? ??????????- ?????? ?????????? ????? ?? MILD
  LT HEMIPARESIS
• ?????? ?????- ??? ???? ????
• TEE PFO, ??? RT to LT ???, ??? ???? ? SBE, ??
  ????? ?????? ????? ???
• 27.12.06- ????? ????? ( III )- ??? ????? 180 ??,
  ????, WBC 92, LYM 88, PMN 12, GLU 25, PROT 118

43
????? ?????

• ????? ????( 8.01.06 )- ??? ????? ???????????
  ?????????, ?? ?????? ??????
• ?????? ??????????- BILATERAL ABDUCENS PALSY,
  ????? ??? ???? ???? ????, ????? ????????? ?? ???
  ????, ?????????? LT gt RT , RT TRUNCAL ATAXIA .

44
? 6.01.06 ????? ??? MRI ???
45
????? ?????

• ???? ????? ???? ?????-
• RIFAMPIN, PYRAZINAMIDE
• STREPTOMYCINE, TAVANIC
• ????? ????? ?? ????????? ?? 50 ?"? ????.

46
Cryptococcal meningitis

• Cryptococcal meningitis - the history is longer
  (ie, months) than that of tuberculous meningitis,
  and perivascular cysts often are seen in the
  region of the basal ganglia.
• Perivascular cysts do not occur with tuberculosis

47
Cryptococcus neoformans

• Occurs worldwide in soil and
• in bird droppings
• Prominent feature thick polysaccharide capsule,
  which causes evasion from phagocytosis

48
EPIDEMIOLOGY OF CRYPTOCOCCOSIS

• Infection is always exogenous, is not transmitted
  from human to human

49
CRYPTOCOCCAL MENINGITIS
50
CRYPTOCOCCAL MENINGITIS

• Prior to the discovery of amphotericin B in 1955,
  80 of patients with CNS involvement died within
  2 years of diagnosis
• Cryptococcal CNS infections usually involve both
  the brain and meninges, causing diffuse disease.
• Immunocompetent hosts may present with either
  meningitis or focal cryptococcomas

51
CRYPTOCOCCAL MENINGITIS

• CSF- protein elevation, mononuclear pleocytosis,
  hypo glycorrhachia
• Fungal CSF culture-gold standard
• India-ink smear insensitive-25-50
• CSF cryptococcal antigen-sensitivity gt90, Blood
  Cr Aggt75

52
Cryptoccocal meningitis CSF Indian ink
examination
53
TREATMENT OF CRYPTOCOCCL MENINGITIS

• Patients with HIV-amphotericin B for 2 weeks,
  with or without 2 weeks of flucytosine followed
  by fluconazole minimum of 10 weeks.

54
NEOPLASTIC MENINGITIS( NM )

• multifocal seeding of the leptomeninges by
  malignant cells is called Leptomeningial
  Carcinomatosis if the primary is a solid tumor,
  and lymphomatous meningitis or leukemic
  meningitis if the primary is not a solid tumor.

55
NM

• 1-8 of patients with CA- LC.
• The most frequent origin - Among solid tumors,
  adenocarcinomas
• breast cancer - 11-64 of patients with LM,
  followed by lung cancer (14-29), melanoma
  (6-18), and gastrointestinal cancers (4-14).
  Primary brain tumors, especially medulloblastomas
  and high-grade gliomas, also have a tendency for
  cerebrospinal fluid (CSF) spread.
• Wen and Fine 1997 Kesari and Batchelor 2003

56
EPIDEMIOLOGY OF NM ( LM )

• The incidence of LM in adults with ALL remains
  high, despite similar prophylactic measures.
• Patients with AML - 20-50 risk of meningeal
  involvement
• LM is uncommon in patients with CML and hairy
  cell leukemia.
• LM is present in up to 50 of patients with CLL
  at autopsy, although it is almost always
  asymptomatic during life (Grossman and Moynihan
  1991).
• NHL-6
• LM is rare in patients with Hodgkin's disease
  and multiple myeloma (Grossman and Moynihan 1991)

57
NM

• headache, lethargy, papilledema, behavior
  changes, and gait disturbance (the latter can be
  due to either cerebellar or cauda equina
  involvement
• Cranial-nerve involvement -94 impaired vision,
  diplopia (most common), hearing loss, and sensory
  deficits, including vertigo. Solid tumorderived
  LC has a higher affinity for the optic and
  extraocular nerves, while leukemic meningitis
  preferentially affects the facial nerve.
• Spinal-root involvement is caused by either
  meningeal irritation or invasion of the spinal
  roots.. Spinal-root symptoms are usually followed
  by cranial-nerve symptoms.

58
DIAGNOSIS OF NM

• 50 of patients with LC - abnormal imaging
  findings contrast enhancement of the basilar
  cisterns, cortical convexities, cauda equina, or
  hydrocephalus without a mass legion.
• this enhancement usually follows positive
  cytologic findings by 6 months

59
NM
60
MRI IN NM
61
DIAGNOSIS OF NM

• Carcinoma cells in the CSF is diagnostic, few
  false-positive results in patients who have
  reactive lymphocytes
• negative cytologic findings do not rule out the
  diagnosis, as 50 of patients with LC have a
  negative cytologic result on the first LP, 15
  after 3 high-volume LPs.

62
DIAGNOSIS OF NM

• CSF pleocytosis , protein elevations , reduced
  glucose levels
• Xanthochromia -LC from a melanoma
• Biochemical markers in CSF

63
TREATMENT OF NM

• Radiation therapy to sites of symptomatic and
  bulky disease
• Intrathecal chemotherapy 
•  Methotrexate (10 mg twice weekly) leucovorin 
•  Thiotepa (10 mg twice weekly)  
• Cytarabine (50 mg twice weekly)
•   Cytarabine (DepoCyt) (50 mg every 2 weeks)
• Systemic chemotherapy (e.g., high-dose
  methotrexate)
• Optimal treatment of systemic disease

64
PROGNOSIS OF NM

• Among patients with LC from solid tumors, the
  best response to chemotherapy and radiation - LC
  from breast cancer, with 60 improving or
  stabilizing and a median survival of 7 months
  15 survive for a year
• 40 of LCs from small-cell lung carcinoma improve
  or stabilize, and patients with this disease have
  a median survival of only 4 months.
• Melanoma-derived LC - 3.6-month median survival,
  and only 20 of these patients stabilize or
  improve with treatment.
• Nonresponders to chemotherapy seldom survive
  longer than a month.

65
????? ?????

• CT ??? ???? ( 15.01.06)- ???? ????- ???? ???? ?
  LUL.
• ????? ????? ( IV ) 9.1.06- ??? ????? 200 ??"
  ????, ???? ????, WBC 316, PMN 24, LYM 76, GLU
  44, PROT 113
• INDIA- INK ?????, CRYPTOCOCCAL AG ?????,????
  ????? ????? ?? ?????
• CYTO SPIN- T CELLS ???????????? ????? ??????
  ?????
• EEG ?????? ?????????? ??? ?? ????? ???? ??????.
  ?????? ????? ??? ?? ????? ???? ???????

66

• ????? ????????? ?? CSF ( 9.01.06
  27.12.06 5.02.06 ) ?????????? ??????? ,
  ?????????????????, ??? ???? ???????
• CT ??? ??? ???? ????? ( 8.01.06)-??????
  ?????????? ????? ???????? ????? ?????, ???????
  ???????? ????????

67
????? ?????

• ????? ??? ?????? ?????- ????
• HIV- ?????
• OB ? CSF ?? ?????
• VDRL ??? ? ? CSF- ?????
• ???????? ? LYME, BRUCELLA,Q FEVER, TOXOPLASMA
  ?????
• CRYPTOCOCCAL AG ??? ? ? CSF- ?????

68
????? ?????

• ACE ??? ?? CSF- ????
• ?????? ?? ?????
• PPD ?????
• ?????? ???? ??????? ??????
• ?????? ?? ?????? ?????- ??????

69
NEUROSARCOIDOSIS

• CSF abnormalities 80 protein elevation
  lymphocytic pleocytosis- 81, 55- OB, CSF ACE
  abnormally high in 33
• Kveim-Siltzback skin reaction- no longer available

70
MRI IN NEUROSARCOIDOSIS

• white-matter lesions,
• hydrocephalus,
• mass lesions in the brain parenchyma,
• meningeal enhancement, enhancement of
  parenchymal lesions and lesions of the optic
  nerves and spinal cord, with or without
  enlargement of these structures

71
MRI IN NEUROSARCOIDOSIS
72
NEUROSARCOIDOSIS

• Biopsy-sarcoid granulomas lymph nodes ,bones
  ,uvea ,skin, muscle
• Radionuclide scanning with gallium-uptake in the
  chest, spleen, salivary or lacrimal glands-50
• Hypercalcemia ,elevated ESR, anemia,lymphocytopeni
  a, hyperglobulinemia-in active disease

73
TREATMENT OF NEUROSARCOIDOSIS

• 50-spontaneous remission
• Indications for steroid therapy-disabling
  syndrome or recent onset of neurologic symptoms
• Steroides and / or immunomodulating treatment
  ( metotrexate, cyclosporine)

74
ISOLATED CNS ANGIITIS

• classic picture is one of progressive,
  cumulative, and multifocal neurological
  dysfunction
• exceptions- presentation suggests cerebral
  tumor, chronic meningitis, demyelinating disease,
  acute encephalitis, myelopathy, simple dementia,
  and degenerative disorders
• When isolated CNS angiitis presents as a stroke,
  it is usually because of intracerebral
  hemorrhage, which occurs in approximately 15 of
  patients at some time in the illness.

75
ISOLATED CNS ANGIITIS

• headache and confusion are the most common
  presentation
• Virtually every neurological sign or symptom has
  been reported at least once
• Systemic symptoms are generally absent

76
Pathology of Isolated Central Nervous System
Vasculitis

• The vascular inflammation is usually of a chronic
  granulomatous nature, with monocytes and
  histiocytes, lymphocytes, and plasma cells
  infiltrating the walls of small (200 µm) arteries
  and veins, particularly in the leptomeninges

77
Pathology of Isolated Central Nervous System
Vasculitis

• giant cells are not required to make a diagnosis
• no predilection for bifurcations
• eosinophils are not present in large numbers

78
Laboratory Findings in Isolated Central Nervous
System Vasculitis

• the CSF has been abnormal in almost all
  autopsy-documented cases
• the abnormalities are nonspecific, namely a mild
  lymphocytic pleocytosis and a mild to moderate
  elevation in protein. Oligoclonal bands and
  elevated immunoglobulin (Ig)G index are
  occasionally encountered, as are low glucose
  values and leukocyte counts of several hundred
  per µl.

79
Laboratory Findings in Isolated Central Nervous
System Vasculitis

• cerebral angiography has been entirely normal in
  many pathologically documented cases,
• the arteriographic changes of vasculitis, when
  seen, are not specific (Alhalabi and Moore 1994).
• Given its lower spatial resolution, MR A is
  unlikely to be useful.

80
ISOLATED CNS VASCULITIS
81
ISOLATED CNS VASCULITIS

• Diagnosis is made most often by brain biopsy
  sample of meninges
• Only 50 -typical histopathological changes

82
????? ?????

• CSF ????? ?????? PCR ?????, PANFUNGAL AG ( 28S r
  RNA), PANBACTERIAL AG( 16S r RNA)
• ???? ????? ??????????? ? FLUCONAZOLE
• ????? ????-??????? ????? ???? ????? PCR ??????
• PCR ?????- ?????

83
????? ?????

• ????? ????? (V ) 5.02.06- ??? ????? 160, WBC 93,
  LYM 88, GLU 42, PROT 74
• CT ??? ??? ??? ???? ?????
• ( 2.02.06)- ??? ???? ??? , ??? ??????? ???????
  ?????? ????? ( ??? ?????? ?????? ?????)
• ????? ?????- ?????

84
????? III

• ????? ????? ????? ( 6.02.06 )?? ????? ???? ??????
  ?????????? ??? ????????, ???? ???? ???, ????? ??
  ????? ?? ?????.
• ???? ????? ???? ????? ?????????? 50 ?"?

85
????? ?????

• ???? ?????? ???? ????? ?????????? ????? ?????
  ?????? ?????? ?????
• ????? ????- ????? ????? ?????- ????? ?????
  ???????????? ???????, ???? ????? ????????
  ?????????????
• ?????( 22.05.06) ???? ???? ???, ????? ? ??
  ??????, ????????, ????? ?????? ???? ???? ??? ?????

86
????? ?????

• CT ??? ( 24.05.06)-3 ??????? ??????? ????? ????
  ?????, ????? ??????? ???????? ????, ? RT CPA, ???
  ????? ?????.
• EEG ???? ?????, ??? , ?? ???????.
• ????? ????? ???????? ?????????????
• ???? MRI ???

87
(No Transcript)
88
(No Transcript)
89
(No Transcript)
90
????? ?????

• ? 4.06.06 ????? ??? ???????? ???? ? OBEX, ????
  ???, ???? ????? ?????????- ???? ???? ?????? ???-
  ????? ???????
• ??? ???????????? ? ISONIAZID ????? ????? ????
  ????? ? 6 ???? ????????????, ???? ?????????? ?
  7.06.06

91
????? ?????

• ? 13.6 ? ? 27.6 ??? CT ??? ??? ??? ?.? ??????
  ????? ????- ??????? ??? ???????? ?????????????
• 9 ???? ???? ???????- ???, ???????? ?????- ????
  ????? ?????? ? MEROPINEM ? VANCOMYCIN ???? ?????
  ???? ???? ???- ???????

92
????? ?????

• ??? ????? ????? ???? ???? ?? ????? ??????????-
  ???? ????? ? DRUG INDUCED FEVER/paradoxical
  reaction
• ????? ???????????? ?????? ????? ?????? ?????.

93
????? ?????

• ? 21.08.06 ????? ???????? ???
• ?????, ????? ??? ?????? ??????, ?????? ??????,
  ????????, ????? ??????????- ??? ????
• ?????? ??????????- ????? ??????? ?????? ???
  ???????? , ???? ????? ?????? ?????????, MILD LT
  HEMIPARESIS, RT TRUNCAL ATAXIA, ???????? ???
  ?????? ???-??? ?????

94
????? ?????

• CT ??? ??? ??? ???? ????? 24.08.06- ????? ?????
  ???, ????? ?? ????????? ?????? ????? ?? RT CPA
• ????? ????? (27.08.06 )-??? ????? 230 ??" ????,
  WBC 99, PMN 62, PROT 131, GLU 38
• ????? ?????( 5.09.06)- GLU 24, PROT 125, WBC 182,
  LYM 76

95
(No Transcript)
96
(No Transcript)
97
?? ????? ??????? ?????? ?????????? ?

• ?????? WERNICKE ( ??? ????? ?????? )- ????? ????
  ????? ? IV THIAMINE ??? ????? ???????
• ????? ? HYPOTHYROIDISM- ??? ????? TSH ???? ????
  ?? ELTROXIN ??? ????? ?????
• ????? ??????????- ????? ,?? ?????? ?????? ??
  ?????? ??????, ????? ??????????, ????????,???
  ????? ???? ???????? ???????, ????? ????? ? CT ???
  ??? ????? ??????? ??????- ????? ??????

98
HYDROCEPHALUS IN TB MENINGTIS

• Hydrocephalus occurs in most patients who survive
  the first 4-8 weeks.
• Hydrocephalus may be communicating due to
  obstruction of the arachnoid granulations, or it
  may result from obstruction of the cerebral
  aqueduct or fourth ventricular foramina by
  tuberculous exudate in the acute phase and by
  pachymeningitis in the chronic phase of the
  disease

99
HYDROCEPHALUS IN TBM

• 31- requiring neurosurgery procedure
• the presence of cerebellar symptoms or signs may
  be useful in alerting the clinician about the
  existence of hydrocephalus
• QJM, 2003, vol. 96, no9, pp. 643-648 

100
HYDROCEPHALUS IN TBM

• The timing of the VPS procedure and cerebral
  complications have an effect on the final
  outcome.
• Early VPS gave a better outcome in mild and
  moderate hydrocephalus
• Pediatric neurosurgery,   2002, vol. 37, no4, pp. 
  194-198 

101
????? ?????

• ???? ???? ??????? ??????? ?? ????? ? 30 ??" CSF
  ?? ????? ???? ?????? ??????????
• ???? CONTINIOUS CSF DRENAGE ( 6.09.06- 12.09.06)-
  ????? ??????
• ????? ????? ?? DEXACORT ?? 12 ??"

102
????? ?????

• ???? MRI ???( 16.9.6, ???? ???) ?????? ????????
  ????? ??? ?????( ?? ??????????). ????? ?????
  ????? ???? ??????? ??? ????? ??????. ????? ??????
  ?? ??????? ?????? ?????? ????????? ????
  ???????????. ??? ????? ?????.
• EEG ???? ????? ??? ???? ???????
• ????????? CSF ( 27.08.06, 5.09.06)- ??? ????
  ????? ???????.
• ?????? CSF- ?????

103
(No Transcript)
104
????? ?????

• ?????? ?????? ?? ???? ????????????- ???? ????? VP
  SHUNT
• ????? ???????- ????, ??? ?????, ????? ???????.
• CSF ??? ???? ??? ??????- WBC 34, LY 94, PROT
  123, GLU 32

105
?????

• ????? ???? ??? ????? ?????

106

• Tuberculous meningitis is a rare, treatable
  neurologic disorder, in which early recognition
  is paramount because outcome depends greatly on
  the speed with which therapy is initiated

107
(No Transcript)