Cerebellar Diseases - PowerPoint by fjwuxn

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  SEMINAR -SEP 29/2006
• Derived from the somatic afferent portion of the alar plate
• acts as a monitor or modulator of motor activity
  "originating" in other brain centers.
• One of the major cerebellar functions is automatic
  excitation of antagonist muscles at the end of a movement
  with simultaneous inhibition of the agonist muscles that
  initiated the movement.
• cerebellum is located in the posterior fossa of the skull,
  dorsal to pons and medulla oblongata and separated from
  the occipital lobes by the tentorium cerebelli.
• On coronal planes has two portions the midline, vermis
  and cerebellar hemispheres.
• vermis - older- receives mainly spinocerebellar afferents
• Hemispheres have more complex fiber connections
Histologically. the cerebellar cortex has 3 layers:
•  the outer - molecular layer , the middle - Purkinje cell
  layer , the inner most - granule cell layer
• - five cell types are distributed in these layers
outer basket cell and inner stellate cells in the molecular
  layer: purkinjie cells arranged in a single row , granule
  and Golgi cells in granule cell layer
• - The white matter of the cerebellum is made up of
  intrinsic, afferent, and efferent fibers.
• - 4 pairs of nuclei on each side of the midline with in the
  white matter core of the cerebellum receive input from the
  cerebellar cortex and incoming afferents and cerebellar
• Fastgial nucleus,nucleus globose, nucleus emboli form
  and dentate (lateral cerebellar) nucleus.
considering connections of these nuclie and sagital organization,
  the cerebellum can be divided longitudinally
         a) midline (vermal ) zone - contain cerebellar neurons
      projecting    to        the   fastigial  nucleus.    Abnormal
  stance,gait,truncal      titubation,disturbance  of   extraoccular
         b) an intermediate (paravermal) zone contain neuron
       projecting to the nucleus interposed
         c) the lateral (hemisphere) zone contain neuron projecting to
       the dentate nucleus. Similar Sx plus decomposition of
   - Each nucleus controls a different type of mode of
• inferior and superior cerebellar peduncles are afferents and efferents.
• Inferior cerebellar peduncle connects cerebellum to medulla oblongata.
   dorsal spinocerbellar tract (T1-L2) , cuneocerebellar tract ,
   vestibulocerbillar tract , reticulo cerebellar tract , trigeminocerebellar tract
Efferent :fastigiobulbar,cerebelloreticular,
Middle cerebellar pudncle:cotcopontocerebellar tracts
Superior cerebellar pud-cerebellum to midbrain
           mainly efferents
 - accompanies acute, less often in chronic
 - ipsilateral
 - more noticeable in the upper limbs- proximal muscles
 - decreased resistance to passive stretch of muscles
 - Occurs in neocerebellar lesions.
Ataxia or Dystaxia
 - result from defective timing of sequential contractions
  of agonist and antagonist muscles.
 - due to disturbance in the smooth performance of
  voluntary motor acts.
 - movements errantic in speed, range, force, and timing
 - due to absence of cerbellar inhibitory and modulating
 - ataxia may affect limbs, trunk, gait, may be acute onset
  ,episodic or progressive - ataxia includes asynergia
  (dysdiadokinesia, past pointing, excessive rebound
 - Wide based stance and gait characterized by staggering
  and impaired tandem walking.
 - Truncal instability -falls in any directions.
 - Titubation or truncal ataxia suggest midline cerebella
cerebellar dysarthria
   abnormality in articulation and prosody
   described as scanning, slurring, staccato,
    explosive, hesistant, garbled.
   specially lesion of dentate nucleus gives
    kinetic (intention) tremor. because intrupt
    rubro-olivo-cerebellar circuit
   static (postral) tremor also may ccur.
    • frequently
    • gaze   evoked,      upbeat,     rebound
Nonmotor manifestations.
  cerebellar   cognitive   affective    syndrome-
   characterized    by     impaired        executive
   functioning, personality changes associated
   with blunted affect or disinherited and
   inappropriate    behavior      ,     visuospatial
   disorganization,     impaired      visual-spatial
   memory, mild anomia, agrammatism and
   macrographia
Rostral vermis syndrome
         • - Wide based stance and gait
         • - ataxia of gait- little ataxia on heel to shin manuever
         • - Normal or only slightly impaired arm coordination
         • - Infrequent presence of hypotonia, nustagmus, and dysarthria.
                in chronic alcoholic patients.
         • - remarkable purikinje cell loss
caudal vermis syndrome
         • - axial disequilibrium and staggering gait,
         • - little or no limb ataxia,
         • - spontaneous nystagmus and rotated postures or head.
         • - seen in damage of flocculondular lobe especially medulloblastoma in
           children as it grows superimposed neocerebellum
cerbellar hemispheric syndrome
         • - typically incoordination of ipsilateral appendicular movements.
         • - affects muscles involved in speech and finger movements etiologies- in
           farcts, neoplasm and abscess
pancerbellar syndrome
         • - combination of all other cerebellar syndromes
         • - characterized by bilateral signs of cerebellar dysfunction affecting the
           trunck, limbs, and cranial musculature.
         • etilogy - ifections, parainfections, hypogycemia, hyperthermia,
           paraneoplastic disorders, toxic metabolic disorder.
      Careful Hx/P/E accurate Dx and appropriate Mx
      Age of onset
      Tempo of progression,associated neurologic and systemic signs
      Family Hx,ethinic origin, country
      True cerebellar ataxia Vs ataxia associated with vestibular or
       labyrinthine disease- associated with dizziness or vertigo ,
       sensory disturbance (Roberg sign)
      Rate and pattern of development of cerebellar symptoms help
       to narrow ddx
      Gradual, progressive, bilateral, symmetric - Biochemical,
       metabolic, immune, or toxic etiology.
      Focal, unilateral Sx with headache and impaired level of
       consciousness with ipisilateral cranial nerve palsy and
       cotralateral weakness imply a space-occupying cerebellar
symmetric ataxia
   progressive, symmetiric reclassified with
    respect to onset as acute (over hours or days)
    subacute (weeks or months) or chronic
    (months of yrs.)
   acute /Reversible ataxia intoxication with
    alcohol, phenytoin, lithium, barbiturates.
   subacute degeneration of cerebellar vermis
    due to combined effect of alcoholism and
    malnutrition. deficiency of B1 and B12
    vitamins,    hyponatremia     ,paraneoplastic,
   Chronic symmetric inherited ataxia metabolic
    disorder hypothyroidism, chronic infections
    meningovascular syphilis
Focal ataxia
    acute focal- ischemic infarction, cerebellar
    - ipsilateral to the injury
    - may be associated with impaired level of
     consciousness due to BS compression or ↑ ICP
    ipsilateral pontine sugns (CN, VI and VII palsy)
    - posterior fossa subdural hematoma, bacterial
     abcess, primary or metastatic cerebellar tumor.
    - CT or MRI
    - most true neurologic emergencies / sudden
    - acute surgical decompression may be required
    - acute or subacute focal cerebellar syndrome in
     AIDS are lymphoma or PML.
    - chronic focal - MS, Chiari malfo, congenital cyst
     of posterior fossa (Dandy -Walker syndrome)
Focal and and Progressive Signs
SymmetricIpsilateral Cerebellar Signs

 Acute (Hours to          Subacute (Days to       Chronic (Months to      Acute (Hours to          Subacute (Days to        Chronic (Months to
 Days)                    Weeks)                  Years)                  Days)                    Weeks)                   Years)

 Intoxication: alcohol,   Intoxication:           Paraneoplastic          Vascular: cerebellar     Neoplastic: cerebellar   Stable gliosis
 lithium,                 mercury, solvents,      syndrome                infarction,              glioma or metastatic     secondary to vascular
 diphenylhydantoin,       gasoline, glue;         Anti-gliadin antibody   hemorrhage, or           tumor (positive for      lesion or
 barbiturates (positive   cytotoxic               syndrome                subdural hematoma        neoplasm on              demyelinating plaque
 history and              chemotherapeutic        Hypothyroidism          Infectious: cerebellar   MRI/CT)                  (stable lesion on
 toxicology screen)       drugs                   Inherited diseases      abscess (positive        Demyelinating:           MRI/CT older than
 Acute viral              Alcoholic-nutritional   Tabes dorsalis          mass lesion on           multiple sclerosis       several months)
 cerebellitis (CSF        (vitamin B1 and B12     (tertiary syphilis)     MRI/CT, positive         (history, CSF, and       Congenital lesion:
 supportive of acute      deficiency)             Phenytoin toxicity      history in support of    MRI are consistent)      Chiari or Dandy-
 viral infection)         Lyme disease                                    lesion)                  AIDS-related             Walker
 Postinfection                                                                                     multifocal               malformations
 syndrome                                                                                          leukoencephalopathy      (malformation noted
                                                                                                   (positive HIV test       on MRI/CT)
                                                                                                   and CD4+ cell count
                                                                                                   for AIDS)

 Abbreviations: CSF, cerebrospinal fluid; CT, computed tomography; MRI, magnetic resonance imaging.
         CBC
         ESR,U/A,CXR,
         CSF-
         Serology-HIV,toxo,AntiYo,Ri,Hu,GAD,gladian

     special test
         Toxicology-matals,drugs(blood,urine)
         ECG,ECHO,NCS
         IMAGING-CT,MRI,U/S,
         Genetics
- result of insult to the cerebellum and its connecting pathways.
- - Acquired, Inherited, Sporadic ataxia

Acquired ataxias
• - In many progressive ataxia result from environmental insults

 Hypothyroidism - occasionally -mild gait ataxia in conjunction with
• - its systemic symptoms
• - TFT needed in patient with progressive ataxia
• Dx - clinical + TFT
• Rx replacement
Hypoxia damages Purkinje cells-ataxi ,myoclonus may result
Hyperthermia damage purknije cells
Hyperammonia in child
Wilsons dx-tremor,dystonia; Rx is copper restriction ,chelation
     -The major exogenous agent causing ataxia
  significant proportion f alcoholics have
  midline cerebellar degeneration at autopsy.
 -     characterized     by    progressive   gait
 disturbance of a cerebellar type with little in
 the way of upper limb ataxia, speech
 difficulties, or eye movements abnormalities
 (relative sparing of cerebellar hemispheres
 - Imaging- typical vermial atrophy.
  -Chronic alcoholism - significant cerebellar
 atrophy (1% severe alcoholics)
 - Adverse effect of 5- FU (used in breast and GI
 - Conventional dose of 5-FV may cause cerebellar
 ataxia if there is an abnormality of pyrimidine
 dehydrogenase deficiency.
 - Higher dose 5-FU - pancerebellar syndrome
 (acute or sub acute coarse)
 - cytosine arabinoside in high dose ( 3 gm/m2 for
 8-12 doses- conventional dose 1000-2000 mg/m2
 for 5-7 days) significant pts develop cerebellar
 syndrome. Pathologically characterized by loss of
 Purkinje cells, gliosis , loss of dentate neurons,
 and spongiform changes.
  Organic     mercury    contamination      from
  mercury -containg fungicides.
  - Mercury toxic cerebellar granule cells and
  visual cortex.
  - causes parasthesia, ataxia, restricted visual
  Manganese- Parkinson + ataxia
  Bismuth- gait ataxia, confusion. mycoclonus
  - chronic solvents abuse (esp. toluene)
  - spray paint
  - paint thinners
  - Issue of cerebellar atrophy and anticonvulsant
  (phenytoin) is controversial.
  - Transient cerebellar signs in supratherapetic
  dose many anticonvulsants seen.
  - Persistent ataxia and purkinje cell loss seen
  prolonged phenytoin use
  - Pathogenesis is unclear     - Hypothesis direct
  toxic effect of phenytoin, a result of repeated
  hypoxia related seizures, the effect of seizure
  related electrical discharge on cerebellar
  Purkinje cells.
  - avoid phenytoin in an epileptic patient if ataxia
  /cerebellar atrophy present.
•        may be feature of post infectious encephalomyelitis but
   usually accompanies more diffuse cerebral process.
•       In children restricted cerebellar syndromes seen when
   acute ataxic disorder that is not associated with a more diffuse
   process reflected by seizures, meningismus or obtundation.
•       In most children preceded by a non specific viral syndrome
   or varicella-peak incidence 5-6yr.
•        similar picture from EBV in teenage years.
•       Dx CSF protein elevation and modest mononuclear
   pleocytosis and MRI -signal density changes in the cerebellum.
•       Px - excellent.
•        Brain stem encephalitis - ataxia ophtalmoplegia and other
   lower cranial nerve palsies- resemble MFS of GBS
- Many neurologic syndrome - ataxia
- Most pts have focal lesions, like
  lymphoma,      chronic    meningeal
  infection, PML or toxoplasmosis.
- 30% ADC - have ataxia prior
- MRI - cerebellar atrophy
- Pathology - marked granule cell
- progressive ataxia.
- Rapidly progressive dementing illness.
 - Due to accumulation of mutant prion protein (result from
   post translational modification of normal prion protein)
- Among CJD - 17% early ataxia 60% cerebellar pathology
   at autopsy.
- Upper motor neuron signs are common,
- myclonus -25% and dementia evolves late.
- Survival 7wk - 8 years
- Pathological- cerebellum shows striking granule cell loss
- Dx - protein 14-3-3 in CSF and coden 29 homozygosisty
   tall-by ELISA
                  •   Autoimmune causes of ataxia
Paraneoplastic cerebellar degeneration syndrome
    that reaches its nadir with in a few months of onset.
    Produces severe ataxia wit dysarthria and oscillopsia, diplopia,
   vertigo other neurologic sn-dementia, extra pyramidal signs, hearing
   loss, dysphagia.
     MRI- typically-cerebellar atrophy and high density signal in deep
   white matter.
 CSF- mononuclear pleocytosis and oligoclonal bands.
 The syndrome results from autoimmune process triggered by the
 Anti Yo in ovarian ca
 Anti-Hu. Ab. in SCLC.
 Purkinjec cell degeneration in 25 % with Anti.Hu.Ab.
 Anti Ri Ab - truncal ataxia and opsoclonus in breast cancer.
Ataxia with Gluten Sensitivity
•    Seen as neurological complication in celiac disease 68% had
    antigliadin Ab.
•    Slowly progressing ataxia associated with brisk tendon reflexes,
    peripheral neuropathy, cognitive changes, mycolonus.
•    Pathology - cerebellar Purkinje cell loss, infiltration by Tcell
    lymphocyte, posterior column degeneration
•    Variable proportion show celiac sprue on duodenal Bx.
•    Whether gluten -free diet or other immunomodulation will
    improve gliadin Ab- associated ataxia is unclear.
Ataxia and antiglutamate decarboxylase antibodies.
• - Recently reported Anti GAD in progressive ataxia.
• - Usually middle aged women - associated with peripheral
   neuropathy, slow saccades, stiff- person syndrome.
• - Many pts had multiple organ specific Ab including Ab to
   thyroid cell, pancreatic islet cell,
• Abs are seen in higher titers in adult onset diabetes and
   cerebellar purkinje cells.

Nutritional vit E deficiency
•   Rare
•   In some lipid malabsorption eg. In cystic fibrosis,cholestatic dx

Demyelinating (ms)
• - clinical feature other CNS involvement CSF findings
 Lesions –cerebellum or pathways
 Infarction - thrombotic or embolic occlusion of cerbellar vessels
 clinical manifestation depends on specific vessels involved and
  extent of collateral circulation
 main symptoms vertigo dizziness, nausea, vomitting gait
  unsteadiness, limb clumsiness, headache dysarthria, diplopia
  and decreased alertness, nystagmus.

  2 clinical syndromes - cerebellar infarcts with fourth
  ventricular and brainstem compression and those without.
 Large cerebellar infarcts - cause brainstem compression with
  onset of occipital headache, vertigo, nausea, vomiting gait, and
  dysarthria       impaired      consciousness.       Obstructive
  hydrocephalus, upward or down ward hernia tion.
 small (border zone) infarcts specific boundaries causes cardiac
  arrest4% atheroma or hypercoagulable 20% focal cerebellar
  hypo perfusion occlusion of vertebrobasilar occlusive disease
  (34%), brain embolism (23%)
Mass lesions
• Most common is hemorrhage near dentate nucleus in
   HTN,edema in large infarct, tumors in children-
   medduloblastoma, astrocytoma, ependymoma and
 Adults,-Metastasis of tumor, hemangioblastoma, abscess,
   tuberculomas,other granulomas, toxoplasmosis
• Cerebellar                       hemorrhages                       with
   headache,nausae,vomitting,gait                ataxia,vertigo       are
   common but variable.
• are emergency devastating.
•    notorious for paucity and variability of signs,may present with
   headache alone
•    infections are in or near adjacent structures(OM,mastoditis)
• Hydrocephalus
•   Autosomal dominant, autosomal recessive or maternal (mitochondrial)
• Genomic classification superseded the previous clinical expression based
•   Even though cerebellar manifestations dominate, changes may occur in
   BS, SC, optic nerves, retina and peripheral nerves.
•   So manifestations range from purely cerebellar to mixed syndromes of
   these structural abnormalities. Rarely dementia.
•   Homogenous in dominantly inherited family but different phenotypes may
Autosomal Dominant Ataxia
• - Onset usually in 3rd - 5th decade but variable onset of
• - Disease occurs in each generation of the pedigree, the
  offspring of affected parents 50% risk.
• - The progressive dominant ataxias are labeled SCA,
  followed by a number to denote the chromosomal locus.
•    Some differently named are MJD(SCA3), DRPLA
    (Dentatorubropallidolusysian atrophy),Episodic ataxias
    (EA1, and EA2)
• - Absence of Sx in either parents is rare.
•   But possible because early onset in child and late in
    parent, death of parent early, wrong paternity.
Clinical Features of Dominant Ataxia
- Overall have overlapping clinical features.
- Genetic study is gold standard for Dx & classification
- Gradually progressive ataxia associated with an array of cerebellar signs forms
    the core features of the Dx.
- ataxic gait, dysmetria, dysdiadokinesia, dysarhria, abnormal persuit and
    inaccurate saccades of the eyes, nystagmus.
- Many, not all Dx are associated with clinical signs referable to pathology in CNS
- Occulomotor abnormality - ptosis, gaze palsy, blepharospasm
- some- bulbar deficts- facial atrophy, facial fasciculation, toungue atrophy and
    fasciculation, unable to cough.
- UMN sign - DTR, spasticity, Babniski sign
- Extrapyramidal sign- akinetic rigidity, chorea, athetosis, dystonia
- PN- distal sensory loss and DTR , amyotrophy
- In some cognitive decline and seizure, retinal disease and visual loss.
- loss of ambulation over 10-15 yrs.
Imaging and other lab studies in dominat
• MRI/CT - to exclude many disorders
  causing ataxia - stroke, tumors, ms
• atrophy of cerebellum, +/- atrophy of pons,
  medulla, middle cerebellar peduncles, and
  upper cervical cord.
• Hyperintensity of middle cerebellar atrophy
  and SCA6 isolated cerebellar atrophy
• NCS -axonal polyneuropathy
Neuropathology: SCA1, SCA2, SCA7 wide spread
  pathology loss of Purkinje cells pontine neurons,
  olivary neruons.
• +/- dorsal root ganglion cell, cranial and LMN
  and tracts may be affected.
• Both unstable expansions of repeated nucleotide
  sequences and point mutations seen (CAG repeats
  inherited in heterozygous fashion)
• CAG encodes for glutamine - polyglutamine
• CAG repeats - polyglutamine disorders (ataxin
• Nuclear accumulation of these proteins (normally
  in cytoplasm)
• Ataxins with >40 glutamines toxic to the neurons.
• Ataxin1,2,3,7,atrophin
• EA1 –potassium channel gene mutation on
  chromsome 12
• EA2-calcium channel mutaton on chromosmome
• In some chromosomes or the loci not known
Autosomal Recessive Ataxia
• Most common form of inherited ataxia
• Most of disease begin in childhood or early
  adult life.
• Late onset possible
• Singleton pt- may occur in families.
• Typically parents don't manifest any Sx
  because they are heterozygous for mutation.
• Affects both males and females.
Some of autosomal recessive ataxia
Frederich’s ataxia
Ataxia telangectasia
Ataxia with isolated vit E deficiency
ARA of Charlovox-Sanguenay
Friendreich's Ataxia
• Clinicla Features; prevalence 2/100,000 .
• Age of onset <25 yr. typically early adolescent.
• Onset ↑ing gait difficulty, gait ataxia, loss of
  proprioceptive sense in lower limbs, absent DTR
  (generalized or lower limb) because early involvement of
  dorsal root ganglion cell, dysarthria, UMN sign.

•    Pts loose ambulation by 9-15 yrs after onset. (at this stage
    increasing ataxia in both upper and lower extremities
    profound proprioceptive loss, areflexia, weakness of lower
    limb muscles, dystonia ,flexor spasm and increasing
    dysarthria, dysphagia. Optic athrophy, hearing loss in
•    ECG abnormality and HCMP- 50% pts,
•    Diabetis (10-20%)- insulin resistance and B cell dysfunction,
•    skeletal and spinal deformity common. pescavus, pes equinovarus,
•    Mean age at death 4th decade (cause- cardiac/ respiratory)
•    NCS early absence or reduction of sensory nerve potentials in diffuse
    fashion reflecting loss of large sensory axons of PN
•    Sural nerve Bx loss of myelinated fibers.
•    MRI upper cervical spinal cord atrophy nonmal cerebellum
•    Pathology- loss of Dorsal root ganglion cell,
               - degeneration of dorsal column,
               -degeneration of spinocerebellar and corticospinal tracts,
               -loss of dentate nuclei in cerebellum.
• Mutation in FA is unstable expansion of a
  repeated trinucleotide(GAA) sequence within the
  first intron of the gene X25 on chromosome 9
• or point mutation of the gene (5% heterozygous)
• Pathogenesis
             presence expanded GAA sequence-
  reduced transcription and translational efficiency
  leading to partial deficiency of the protein
• the exact function of ftataxin not clear- is
  mitochondrial iron availability heme synthesis.
Ataxia Telangiectasia
• 3 in million frequency
• Sx/Sn- Present in the first decade of life with progressive telangiectatic
   lesions associated with deficits in cerebellar function and nystagmus
• neurologic manifestations correspond to FA so ddx.
• High incidence of pulmonary infections and lymphatic and RES
• Thymic hypoplasia (Cellular and humoral immunodefinciency)
• Premature aging, endocrine disorders type 1 Dm.
• Increased incidence of lymphomas, HD ,acute leukemias of T-cells,
   and breast cancer.
• Most striking neurologic change: - loss of purkingje, granule and
   basket cells in the cortex and neurons in the deep cerebellar nuclei,
   neuronal loss in olive, loss of anterior horn cells, dorsal root ganglion.
• Gene- ATM gene mutation product protein may result in DNA damage
Mitochondrial Ataxias.
• Each mitochondrion contains several copies of circular
• mtDNA –small and encodes 13 proteins component of
  respiratory chain in oxidative phosphorylation& ATP
• Mt genome inherited maternally
• 30 pathogenic mtDNA point mutations and 60 different
  types of mtDNA deletions are known, several of which
  cause or are associated with ataxia
• Alterations result in reduction in ATP supply,free radical
• Clinical spectrum involves cardiomyophathy and
 Sporadic/ Idiopathic Ataxia
• No primary cause known or no gene
• Progressive cerebellar ataxia resemble IA
• Etiopathogenesis not well known
• Dx is by exclusion of other genetic or
  acquired ataxias
   Eg.sporadic cortical cerebellar atrophy
   spradic ataxia with added noncerebellar
 Most important goal in management of Pts with
  ataxia is to identify treatable disease entities;
 Mass lesions should be ruled out and treated
 Paraneoplastic disorders can often be identified by
  the clinical patterns of the disease that they produce
  ,measurements of specific autoantibody and
  uncovering the primary cancer. (Usually refractory
  but some may respond to tumor removal or
 A number of single case reports improvement after
  tumor removal, plasma exchange, IVIG,
  cyclophosphamide or glucocoticoids.
•    Avoid phenytoin and alcohol.
•    No proven therapy for autosomal dominant ataxia
    (SCA1 - 22 ) - Preliminary evidences that idebenone a free radical
    scavenger, can improve myocardial hypertrophy in pts with classic FA.
    (Not known whether improves neuropathy)
•   Anticholinergic,serotoninergics,GABAergic tried but not effective
•    Acetazolamide - reduce the duration of Sx of episodic ataxia
•    Identifying at risk person's genotype together with appropriate family
    and genetic counseling can reduce the incidence of these cerebellar
    syndromes in future generations.
•    Supportive care of patients with FA include adequate rehabilitation
    efforts aimed at mobility using appropriate device and Monitoring and
    caring of the systemic complications are also important. (Skeletal
    deformty, cardiomyopathy, and dialetes)
•   Avoid Exposure to metals or chemotherapy
•   Gluten free diet
•    Vit E therapy.
•    Vit B1 and Vit B12 Supplementation in
•   Replace hypothyroidism.
•   CSF VDRL (CNS syphilis) Rx
•    Ab titer to Leigionella and Lyme- appropriate
•   Surgery-thalamic stimulation for tremer and brain
•    chemotherapy and radiation for other neoplasms
•   Chelating agents,hemodialysis

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