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EVALUATION AND DIAGNOSIS OF NON COMPRESSIVE MYELOPATHY
PRESENTED BY: DR. HIRDESH CHAWLA
JUNIOR RESIDENT III
COMPRESSIVE
EXTRAMEDULLARY
INTRAMEDULLARY
NON COMPRESSIVE
INFLAMMATORY
NON INFLAMMAT
ORY
Features Compressive Non compressive
Bone deformity + -
Bony tenderness + -
Girdle like sensation + -
Upper level of Sensory loss
+ -
Root pain + -
Onset and progress Gradual May be acute
Bladder and bowel involvement
Early Usually late(early in ATM)
Symmetry Asymmetrical(U shaped)
Symmetrical
TIME COURSE: Acute- within days(usually vascular, radiation, infection) Sub acute- 2-6 weeks Chronic- more than 6 weeks(degenerative, demyelinating , sarcoidosis , dural AV fistula ,
metabolic , tabes dorsalis , HIV related)
PHASE:
Single event(most common) Multiphasic (rare)-Demyelinating, Vascular, Systemic disease
EXTENT OF INVOLVEMENT:
Monofocal- ATM Multifocal-ADEM,NMO,MS
CLASSIFICATION
DISTRIBUTION:
Gray matter-Poliomyelitis White matter-Leucomyelitis Whole cross sectional area-Transverse
myelitis Meninges and SC-Meningomyelitis Meninges and root-Meningoradiculitis
Complete spinal cord: involvement of all the tracts (trauma, compression or acute transverse myelitis).
Brown Séquard syndrome: multiple sclerosis and compression.
Anterior spinal cord syndrome: anterior spinal artery infarct and multiple sclerosis
Posterior spinal cord syndrome: vitamin B12 or copper deficiency.
Central syndrome: spino-thalamic crossing, cortico-spinal and autonomic tracts (syringomyelia, neuromyelitis optica).
Medullary cone: sacral emerging fibres (post-viral myelitis).
Cauda equina: acute cytomegalovirus infection, polyradiculitis
Tractopathies: vitamin B12 deficiency, paraneoplastic myelopathy and multiple sclerosis.
SACD HIV associated myelopathy Freidrich’s ataxia Tabes dorsalis
MYELOPATHY WITH PERIPHERAL NEUROPATHY
1. INFECTIOUS- Viral, Bacterial, Fungal and Parasitic
2. AUTOIMMUNE- SLE, Sjogren’s, Sarcoidosis, Behcet Syndrome ,MCTD, Poly Arteritis Nodosa, p ANCA positive vasculitis.
3. DEMYELINATING- MS,NMO, ADEM, Post viral post vaccinial
4.PARANEOPLASTIC
5. ENCEPHALOMYELITIS
INFLAMMATORY MYELOPATHIES
INHERITED- HSP, Inherited metabolic disorders
METABOLIC- Vit. B12,Copper,folate and Vit. E deficiency. AIDS Associated.
TOXIC –Cassava, Lathyrism, Fluorosis, SMON, Nitrous Oxide
VASCULAR – Ant. Spinal artery thrombosis, AVM, Dural AV fistula
NON INFLAMMATORY MYELOPATHIES
Excludes compressive etiology.
There needs to be gadolinium enhancement of the spinal cord for inflammatory pathology
Brain MRI should be performed to determine if other demyelinating lesions within (CNS) are present ,MS and NMO specific lesions.
NEUROIMAGING
NOT a myelopathy (Guillain Barre’s, Inflammatory radiculopathy)
MRI performed during convalescence period.
Friedreich’s ataxia,
Motor neuron disease,
Vitamin B12 or copper deficiency myelopathy,
Hereditary spastic paraparesis,
HIV,HTLV-1
NORMAL MRI WITH MYELOPATHY
IMAGING FEATURES POTENTIAL DIAGNOSIS
Blood within the spinal cord(bright and dark T1 and T2 signal)
Vascular malformation(cavernous angioma or dural AV fistula)
Flow void within SC Dural AV fistula or AVM
Central T2 signal abnormality Venous hypertension
Ring enhancing lesion Infection or tumour(consider steroids to rule out inflammation process before biopsy)
Fusiform lesion over >3 spinal segments
NMO
T2 bright lesion in white matter ,<2 SC segments,<50% of cord diameter, Rostral caudal extent
MS
Represent extensive involvement of the spinal cord, with abnormal T2 signal traversing at least three vertebral body segments in length.
Differential diagnosis
NMO(typical) Multiple sclerosis- confluent short segment lesions mimicking LESC
Immunological- Neurosarcoidosis,Sjogrens,SLE
Behcet’s disease
Paraneoplastic myelitis
Post infectious
Vascular- Infarction,Dural AV fistula
Metabolic and radiation myelopathy
LONGITUDINAL EXTENSIVE TRANSVERSE MYELITIS
A low CSF glucose concentration:-
infection (fungal, bacterial,or mycobacterial), Isolated low in neurosarcoidosis, carcinomatosis, SLE
CSF WBC count defines inflammatory myelitis.
High immunoglobulin G index in the CSF-Inflammatory
If none of these findings are present at the time of onset of symptoms, MRI and lumbar taps must be repeated two to seven days later.
CSF EXAMINATION
Pleocytosis-Infections, Inflammations, Demyelinating disorders. Mononuclear cells in AV malformations, paraneoplastic
Erythrocytosis- AVM,AVF,SLE,Behcet’s
Elevated protein- Tumours, paraneoplastic, vascular, radiation.
CSF normal-Delayed progressive radiation myelopathy
Bizzare giant cells- vacuaolar myelopathy of HIV.
Pronounced pleocytosis, normal glucose,eosinophilia- schistosomiasis
CSF ANALYSIS
HISTORY AND EXAMINATION S/O MYELOPATHY
NON COMPRESSIVE
INFLAMMATORY
NON INFLAMMA
TORY
COMPRESSIVE
NEUROSURGICAL
EVALUATION OF MYELOPATHY
MRI WITH GADOLINIUM ENHANCEMENT
CSF ANALYSIS
ACUTE TRANSVERSE MYELITIS
Incidence - up to 3 per 100,000 patient years (0.003%) Female preponderance
Typically monophasic (1/4th recur)
First peak between 10-19 yrs of age and other between 30-39 yrs. Of age
Symptoms typically develop over hours to days and then worsen over days to weeks(acute to subacute)
Pyramidal(flaccid paraplegia), sensory(definite sensory level), and autonomic dysfunction to varying degrees .
Backache and progressive paraparesis are presenting complaints.
Early bladder and bowel involvement.
“band like” horizontal area of altered sensation on the TORSO and rarely on neck.(but unlike compressive-no root pain, spinal tenderness).
Plantars are extensor (maybe absent in spinal shock stage)
FEATURES
Diagnostic criteria
CSF IL-6 has been described as a biomarker to help predict disability in acute transverse myelitis
The sensitivity of NMOIgG is 70% whereas the specificity approaches 100%.
MRI findings include focal and central high signal areas in T2 sequences, occupying more than two thirds of the spinal cord axially, and extending over three to four segments, generally in the thoracic spine.
Spinal expansion may or may not be found and, in general, there is contrast medium enhancement, usually patch-like or diffuse.
MRI findings are usually normal in 40% of cases
MRI FINDINGS
INFECTIONS
INFECTIOUS CAUSES
WHEN TO SUSPECT SPINAL CORD INFECTION ?
DEMOGRAPHIC FACTORS – Residence in endemic areas, H/o exposures blood transfusion chemotherapy transplant recipent (CMV,HHV7)
CLINICAL CLUES – other systems – Lymphadenopathy Retina (CMV), Pharynx(EBV), Lung (cryptococcus, TB), Vesicles (HSV, Entero virus 71), Erythema migrans(Lyme’s) and Neurologic- meningoencephalitis, encephalopathy Recurrent genital infections-Behcets
SPINAL CORD INFECTIONS
Enterovirus(Coxsackie and polio),West Nile Anterior horn cells, motor nucleus of brainstem
Herpetic Dorsal root ganglion,extensive inflammatory necrosis of SC
Schistosomiasis causes intensely inflammatory and granulomatous myelitis.Diagnosed by elevated titres of Ab against schistosome.
HSV-2 produces a distinctive syndrome of recurrent sacral cauda equina neuritis(lumbosacral radiculitis) with urinary retention in association with outbreaks of genital herpes (Elsberg’s syndrome)
*Hence disturbance of function are either in sensory or motor NEURONS rather than tracts
SPECIFIC FEATURES
Myelitis that presents as dysfunction of motor and sensory tracts is rarely viral but rather due to Non infectious inflammatory pathology BUT EXCEPTION BEING
Zoster myelitis
HIV associated Vacuolar myelopathy
HAM(Tropical spastic paraparesis)
Dumb rabies
MYELOPATHY can be due to HIV- itself, Herpes Zoster, Tuberculosis, HTLV-1
HIV MYELOPATHY-
DIAGNOSIS OF EXCLUSION Pathologically – vacuolar myelopathy , spongy degeneration ,
demyelination (axons relatively preserved) Most severe in thoracic segments with posterior and lateral columns
affected diffusely SYMMETRIC PAINLESS SPASTIC paraparesis Lesions resemble SACD but B12 levels are normal HAART has no effect on myelopathy
HIV INFECTION
Slowly progressive with UMN signs
Early bladder involvement with disorder of sphincter control.
Upper extremities are spared(except for lively tendon reflexes)
Preserved brainstem and mentation.
Posterior column and corticospinal tract in thoracic cord is most commonly involved.
CSF shows –normal protein and glucose and increased HTLV-1 antibodies
TROPICAL SPASTIC PARAPARESIS BY HTLV-I
Tabes dorsalis ,meningomyelitis, pachymenigitis, spinal vascular syphilis
TABES DORSALIS- less than 5% of neurosyphilis
Post. columns and spinal roots
Preataxic - Lightening pains of the legs, ARP, urinary incontinence
Ataxic phase- sensory ataxia ,slapping gait
Paralytic phase
CSF shows-pleocytosis, increased protein,increase in IgG with OGB, serological tests
SYPHILIS
POST INFECTIOUS AND POST VACCINIAL
• Most common cause of ATM
• Temporal relationship to infection or vaccination
• Development in days to 2 weeks when patient is resolving from febrile epsiode
• Monophasic temporal course
• Varying degrees of weakness, ascending sensory symptoms, sphincter disturbances.
• 40% give a positive H/O infection.(EBV,CMV and Mycoplasma most common. NOT Campylobacter jejuni)
• Slight asymmetric of symptoms and signs, sensory level on trunk and Babinski positive distinguishes it from GBS
POSTINFECIOUS AND POSTVACCINAL
• CSF- WBCs 10 – 100/mm3,Normal glucose, Raised protein ,Pauci inflammatory also. Absent oligoclonal bands
• MRI –Minimal gadolinium enhancement with slight T2 signal abnormalities over 2-3 segments.
POSTVACCINE MYELITIS-occurring in the 3 weeks following a vaccination, such as smallpox ,hepatitis
B, typhoid, influenza, rubella, and tetanus
ADEM-Monophasic disorder that affects the brain and occasionally the spinal cord.
History of preceding viral or other infectious illness.(not definite criteria for diagnosis)
Show diffuse demyelinating lesions that are generally of the same age.
Usually include encephalopathy but may also include focal or multifocal demyelinating inflammatory syndromes of the CNS such as optic neuritis and myelitis.
ADEM is a differential diagnosis for isolated demyelinating syndrome, which is a more common precursor of MS in adults .
ADEM symptoms include rapidly progressing encephalopathy associated with seizures or multiple neurologic deficits.
The spinal cord is affected in 11% to 28% of patients, generally in the thoracic and cervical segments
ACUTE DISSEMINATED ENCEPHALOMYELTIS
There are no diagnostic criteria, but ADEM must be suspected when one or more of the following are present :
•Initial multifocal presentation with multiple symptoms.
• Less than 10 years of age.
• Signs and symptoms of meningoencephalitis.
• Encephalopathy.
• Bilateral optic neuritis.
• CSF pleocytosis without oligoclonal banding.
• MRI shows lesions in areas not affected by MS, such as the grey matter or the cortex.
• Lesions on MRI appear larger with poorly defined edges that enhance with gadolinium
DEMYELINATING DISORDERS
Lesions are usually small (<2 vertebral segments in length) and peripheral.
Cause asymmetric symptoms and signs
Lhermitte sign
Acute spinal MS is relatively painless and without fever and improves with residual signs.
MULTIPLE SCLEROSIS
Polman et al. reviewed McDonald’s diagnostic criteria in 2010 and proposed the following :
Space: One or more lesions with and without gadolinium enhancement in two of the following areas:
periventricular, juxtacortical, infratentorial, or spinal cord.
Time: One new lesion on T2 sequences or a gadolinium enhancing lesion when compared to the previous MR image, and concomitant finding of asymptomatic lesions with or without enhancement.
CSF oligoclonal bands (OCBs) are present in more than 90% of patients(may be absent after first attack)
Immunoglobulin (Ig)G index is seen in more than
60%. following equation: IgG Index -(CSF IgG/albumin)/(serum IgG/albumin). Ratio -0.3 and 0.6
Subclinical optic nerve involvement on visually evoked response testing
Advanced neuroimaging such as diffusion tensor and magnetization transfer imaging may help identify the involvement of the apparently normal white matter, which is abnormal in MS and normal in ADEM.
On the sagittal plane, the plaques may be anterior, central or posterior.
Acute lesions enhance with gadolinium, due to rupture of the blood-brain barrier. This enhancement is less in cerebral lesions.
Unlike neuromyelitis optica, viral or idiopathic myelitis, in MS no black holes are visualized in the spinal cord .
NAA has been has been found to be reduced on spectroscopy, in spinal cord areas that appear normal on conventional MRI.
MRI FINDINGS
Dawson’s fingers on MRI
Lesions are centrally located and necrotic leading to more symmetric symptoms and signs and greater disability
NMO is relatively more common in Asian and African individuals, Female preponderance with mean age of 40 yrs.
Autoimmune conditions including SLE, SjoGren syndrome, and thyroid autoimmune disorders may coexist
NEUROMYELITIS OPTICA
Combination of Optic neuritis with Myelitis also occur in:
Multiple sclerosis ADEM Sjogren’s syndrome SLE Rarely with viral and bacterial
infections. Paraneoplastic (Ab to CRMP 5)
DIFFERENTIALS
Radiological characteristics include a central longitudinal and extensive cervicodorsal lesion (three or more spinal segments) with spinal expansion, of low signal in T1 sequences and high signal in T2 sequences and patchy enhancement.
It has been demonstrated that 60% of patients may have periventricular lesions (areas of high aquaporin 4 concentration).
In this case, NMO is not associated with cerebral white matter lesions, and the spinal lesions are confluent and extend to multiple segments (which is infrequent in MS);
Cranial nerve and cerebellar involvement is common in MS and is not present in NMO.
NMO-IgG -against Aquaporin 4(water channel protein)recently identified serum antibody highly specific (>90%) and sensitive (>70%) for NMO.
Typically oligoclonal bands are absent(unlike in MS)
Acute Demyelinating Disease
MRI SPINE MRI BRAIN CSF
Multiple sclerosis
<2 spinal segments,peripherally located,predilection for posterior and lateral funiculi
White matter lesions, Dawson fingers, juxtacortical, periventricular
OGB and raised IgG index
NMO >3 segments, gadolinium Enhancement and cord swelling.T1 dark lesions and Bright spotty lesions
In 60% of pts. Usually periventricular. sometimes hypothalamic or brainstem
Prominent pleocytosis with PMN or eosinophil predominance, no OGB in 80%, normal IgG index
ADEM Variable lesion length Large, confluent white matter lesions. lesions of same age
Pleocytosis..OGB and IgG index may be abnormal transiently
Idiopathic transverse myelitis
Variable lesion length No brain lesion Pleocytosis..OGB and IgG index may be abnormal transiently
IMMUNOLOGICAL DISORDERS
CNS involvement -5% of cases, 18% with myelopathy
Asymmetrical ascending paraparesis with bladder involvement in most patients.
Subacute or chronic,relapsing , slowly progressive polyradiculopathy , myelopathy
Gadolinium enhancement of active intramedullary lesions.
CSF-increased cells and protein, normal glucose, increased IgG levels and activated histiocytes.
Characterstic lesion is a multifocal-subpial nodular enhancement of meninges adjacent to lesion within the cord or nerve roots.
CXR PA ,ACE levels specificity at 80 to 95 the sensitivity is 60%.Definitive diagnosis requires biopsy.
SARCOIDOSIS
Systemic Lupus Erythematosus -1 to 2% of patients with SLE
The most accepted hypothesis is a vascular mechanism secondary to ischemic lesions
ANA , APLA antibody is positive in 43 to 73% with myelitis
patients with NMO ANA was positive in 52.6%
CSF shows mild lymphocytic pleocytosis. Oligoclonal bands are variable finding
Sjögren’s Syndrome - 35% of cases have spinal cord involvement. Includes episodes of optic neuritis but no oligoclonal bands
PARANEOPLASTIC DISORDERS
Subacute myelopathies
MAY OCCUR BEFORE DETECTION OF CANCER
Amphiphysin- specific antibodies raise the possibility of breast cancer.
Paraneoplastic Disorders and Myelopathy
• Lesions are necrotic involving both grey and white matter
The lesion often involves the thoracic spinal cord extending one or several contiguous segments, that shows a high-intensity signal in T2 sequences and gadolinium enhancement.
In contrast,nodular enhancement seen in intramedullary metastasis or extradural mets. With cord compression
There is increased protein concentration in the CSF with few mononuclear cells. No tumour cells in CSF
• Anti YO, Anti Tr, Anti Hu antibodies, Anti GAD and anti Amphiphysian.
PARANEOPLASTIC MYELOPATHY…
VASCULAR
BLOOD SUPPLY OF SPINAL CORD
Vascular
1% of all strokes, 5% of acute myelopathies
6th to 7th decade
CAUSES: Atherosclerosis , surgery of aorta, systemic hypotension, Iatrogenic causes- vertebral angiography, spinal trauma
Relative hypovascularity of thoracic cord(>60% of SCI occur)
Spinal cord infarction
Pain(often radicular) and sensory symptoms first
Clinical Nadir within 12 hrs
Anterior spinal artery syndrome –symmetric weakness with B/l Spinothalamic with bladder involvement.
Post. spinal artery ischemia –rare Frequent overlap of signs .
Can be devastating and life threatening
FEATURES
Arterial thrombosis: aortic surgery, spinal angiography, vasculitis , embolism, arterial dissection, hypotension, and prothrombotic states.
Anterior spinal artery lesion: anterior spinal syndrome
Posterior spinal artery lesion: posterior column syndrome
Subcommisural artery lesion: Brown Séquard syndrome
Arteriovenous fistula- Weakness with Upright posture or walking
Venous infarct
ETIOLOGY
CSF is normal, although in arteriovenous fistulas there may be higher protein concentrations without pleocytosis .
Spinal MRI shows single central hyperintensity
DIAGNOSIS
Type of vascular lesion MRI findings
Anterior spinal artery occlusion Elongated pencil like lesion in anterior cord
Posterior spinal artery occlusion Triangular lesion in posterior cord
Subcommisural Artery Lateral cord lesion
Hematomyelia Appearance of blood products, Flow voids in the cord
Fibrocartilaginous disc embolism Loss of vertical IV disc height, microfractures in vertebral endplates,T2 signal abnormality
AV fistulas Long spinal cord lesion extending into conus,tortuous vessels.Spinal angiogram needed to confirm
METABOLIC MYELOPATHIES
- Despite widespread screening Vit . B12 deficiency is – 15-25% of older individuals
- ETIOLOGY :- - malabsorptive disorders- atrophic gastritis,- H2 antagonists and metformin, - fish tapeworm
SUBACUTE COMBINED DEGENERATION
Fatigue, generalised weakness
Slowly progresive myelopathy
Mild sensory symptoms with loss of vibration and proprioception sense(POSTERIOR COLUMN)-First manifestation
Paraparesis with hyperreflexia and spasticity(PYRAMIDAL)
Bladder bowel also can occur
Associated PERIPHERAL NEUROPATHY
Psychological symptoms ,cognitive decline
Optic neuropathy
Clinical features
CBC- macrocytosis ,pancytopenia ,MCV (only in 40%)
Vitamin B12 levels –lacks sensitivity and specificity
1/3 rd of cases with normal Vit. B12 levels have elevated homocysteine and MMA levels
Subclinical Vit. B12 deficiency occurs with age
Low levels with neurologic manifestations – cause and effect relation poor
Diagnosis
MRI SPINE –hyperintense T2 WEIGHTED signal in posterior and anterolateral columns without contrast enhancement. INVERTED V SIGN
INVERTED V SIGN
Laughing gas used in anasthesia
N2o interferes with metabolic pathway of methionine synthesis
Symptoms similar to vit. B12 deficiency – usually acute
Myelopathy, neuropathy, myeloneuropathy,impaired cognitive function
More prone in already vit. B12 deficient
Prophylactic use of vit. B12 before anasthesia
Nitrous oxide exposure
CAN alone cause myelopathy (less common)
CAUSES:- Alcoholics GI disease pregnancy drugs – trimethoprim
Myelopathy, neuropathy, optic neuropathy ,cognitive decline
Serum folate ,red cell folate (more reliable) and serum homocysteine levels for diagnosis
FOLATE DEFICIENCY
Posterior and lateral columns are affected with reduced ankle reflexes
Causes- Gastric surgery Zinc toxicity TPN Malabsorption
Hypocupremic anemia with ringed sideroblasts with vacuolated myeloid precursors in marrow mimiking MDS
Clinical -Myelopathy, myeloneuropathy
Diagnosis-serum ceruloplasmin, serum or urinary copper
Copper deficiency
LATHYRISM – Lathyrus sativus ,toxic amino acid(B oxalyl amino alanine) from grass pea
Spastic paraparesis with degenerative changes in spinal cord
Preventable- avoid pure grass consumption, mix with cereals
KONZO- poorly processed cassava
SEEN IN AFRICA
Spastic paraparesis
Toxins
- SMON- clioquinol was used as antiparasitic drug in Japan.
- Subacute paraparesis with optic atrophy. Inevitable death
- ORGANOPHOSPHORUS- CAN CAUSE MYELOPATHY AND MYELONEUROPATHY
- Most imp content –TOCP(Tri ortho cresyl phosphate)
- Acute intoxication f/b latent phase of several weeks
- Progressive leg weakness –sensory motor neuropathy with spacticity paraparesis
- RBC cholinesterase
Chemotherapy induced Hepatic Myelopathy Heroin Myelopathy Fluorosis
Other toxic myelopathies
DEGENERATING MYELOPATHY
FAMILIAL SPASTIC PARAPLEGIA: 3rd – 4th decade. Can occur in 1st decade too
AD/AR/X-linked
Sensory involvement is minimal,Bladder is involved late in the illness.
Amyotrophy, MR, Optic atrophy, cataracts, epilepsy,peripheral neuropathy and deafness
Survival is long because respiration is spared
Only symptomatic therapy
PHYSICAL AGENTS
Amount of current, duration of contact, resistance offered by the skin
Immediate or Delayed – few days to 6 weeks
The deep white matter is the most affected since it comprises the cortex and the subcortical arcuate fibers-when high ampere current flows through body
Heating of tissue, Vasocclusive changes, demyelination, fracture.
Involvement of anterior spinal artery and its branches
SPINAL ATROPHIC PARALYSIS-delayed,focal muscular atrophy. gray matter affected the most.because of low voltage current
Lightening injury:
Arborescent marks
Limbs may be pale and cold or cyanotic
Late presentation of an atrophic limb paralysis Also associated with severe motor polyneuropathy
ELECTRICAL INJURIES
Upper thoracic cord Little or no brain inv. Posterior column > lateral column Decompression in hyperbaric chamber,
Symptomatic treatment
CAISSON’S DISEASE
MC - Mediastinal irradiation for Hodgkin’s disease
Early transient(3 – 6 months after)-Lhermitte sign. Disappear after few months. Spongy appearance of white matter with demyelination.
Delayed progressive/Slowly evolving amyotrophy- Between 12-15 months, sensory followed by motor symptoms
PAIN IS ABSENT(+nt in spinal mets.)
LESION IS EXTENSIVE in rostro caudal fashion than in vascular and demyelinating myelopathy
Coagulative necrosis,vascular changes, secondary degeneration
Could be avoided if 6000 cGy over 30 – 70 days not exceeding 200cGy/day or 900cGy/week
RADIATION MYELOPATHY
• Painful root and cord symptoms
• Syphilis, Resistant meningitis, TB, • Penicillin, Contrast, steroids,
• Thickening of Arachnoid, proliferation of connective tissue and adhesion between arachnoid & dura.
• PERSISTANT PAIN commonly in lumbofemoral regions, but weakness and atrophy are less frequent.
• CT/MRI contrast showing total or partial loss of spinal subarachnoid space(candle guttering).Mri shows loss of normal ring of CSF or localised loculations of CSF
• Degeneration of peripheral fibres of posterior and lateral column
CHRONIC ADHESIVE ARACHNOIDITIS