NEUROLOGY SUBSPECIALTY SEMINAR -SEP 29/2006

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• NEUROLOGY SUBSPECIALTY SEMINAR -SEP 29/2006

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• CEREBELLAR DISEASES

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• ANATOMY
• 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

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• 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 efferent.
• Fastgial nucleus,nucleus globose, nucleus emboli
  form and dentate (lateral cerebellar) nucleus.

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• 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,disturbanc
  e of extraoccular movement
• 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
  movement,dysdiaokinesia,dysarthria,tremer,hypotoni
  a,excessive rebound
• - Each nucleus controls a different type
  of mode of movements.

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• connections
• inferior and superior cerebellar peduncles are
  afferents and efferents.
• Inferior cerebellar peduncle connects cerebellum
  to medulla oblongata.
• afferents
• dorsal spinocerbellar tract (T1-L2) ,
  cuneocerebellar tract , vestibulocerbillar tract
  , reticulo cerebellar tract , trigeminocerebellar
  tract
• Efferent fastigiobulbar,cerebelloreticular,
• Middle cerebellar pudnclecotcopontocerebellar
  tracts
• Superior cerebellar pud-cerebellum to midbrain
• mainly efferents

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• CLINICAL MANIFSTATIONS OF CEREBELLAR DYSFUNCTION
• Hypotonia
• - 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.

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• 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 influences.
• - ataxia may affect limbs, trunk, gait, may be
  acute onset ,episodic or progressive - ataxia
  includes asynergia (dysdiadokinesia, past
  pointing, excessive rebound phenomenon.
• - 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 lesion

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• cerebellar dysarthria
• abnormality in articulation and prosody
• described as scanning, slurring, staccato,
  explosive, hesistant, garbled.
• Tremor
• specially lesion of dentate nucleus gives
  kinetic (intention) tremor. because intrupt
  rubro-olivo-cerebellar circuit
• static (postral) tremor also may ccur.
• Nystagmus
• frequently
• gaze evoked, upbeat, rebound nystagmus

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• 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 dysprosodia
• macrographia

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• 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.

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• APPROACH TO PATIENTS WITH ATAXIC DISORDERS
• 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 lesion.

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• 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, CJD,
• Chronic symmetric inherited ataxia metabolic
  disorder hypothyroidism, chronic infections
  meningovascular syphilis

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• Focal ataxia
• acute focal- ischemic infarction, cerebellar
  hemorrhage
• - 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
  herniation
• - 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)

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Symmetric and Progressive Signs
Focal and Ipsilateral Cerebellar Signs
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• INVESTIGATION
• CBC
• ESR,U/A,CXR,
• CSF-
• protein,VDRL,oligoclonal,PCR,cultu
  re,cytology,
• Serology-HIV,toxo,AntiYo,Ri,Hu,GAD,gladi
  an
• ChemistryOFT,TFT,Parathyroid,RB
  S,electrolyte,Vitamins,special test
• Toxicology-matals,drugs(blood,urine)
• ECG,ECHO,NCS
• IMAGING-CT,MRI,U/S,
• Genetics

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• CEREBELLAR ATAXIAS
• 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
• Hypoparathyroidism
• Hypoglycemia
• Hypoxia damages Purkinje cells-ataxi ,myoclonus
  may result
• Hyperthermia damage purknije cells
• Hyperammonia in child
• Wilsons dx-tremor,dystonia Rx is copper
  restriction ,chelation

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• Toxic
• Alcohol-
• -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)

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• Chemotherapy
• - Adverse effect of 5- FU (used in breast and GI
  cancer)
• - 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.

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• Metals
• Organic mercury contamination from mercury
  -containg fungicides.
• - Mercury toxic cerebellar granule cells and
  visual cortex.
• - causes parasthesia, ataxia, restricted visual
  field.
• Manganese- Parkinson ataxia
• Bismuth- gait ataxia, confusion. mycoclonus
• Solvents
• - chronic solvents abuse (esp. toluene)
• - spray paint
• - paint thinners
•  

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• Anticonvulsants
• - 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.

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• Infections
• 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

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• HIV
• - Many neurologic syndrome - ataxia
• - Most pts have focal lesions, like lymphoma,
  chronic meningeal infection, PML or
  toxoplasmosis.
• - 30 ADC - have ataxia prior dementia
• - MRI - cerebellar atrophy
• - Pathology - marked granule cell loss.

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• CJD
• - 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

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• 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 cancer.
• 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.

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• 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.

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• 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

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• Vascular
• 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)

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• 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,vomitt
  ing,gait ataxia,vertigo are common but variable.
• are emergency devastating.
• Abscesses
• notorious for paucity and variability of
  signs,may present with headache alone
• infections are in or near adjacent
  structures(OM,mastoditis)
• Hydrocephalus

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• INHERITED ATAXIAS
• Autosomal dominant, autosomal recessive or
  maternal (mitochondrial) modes
• 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 occur

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• Autosomal Dominant Ataxia
• - Onset usually in 3rd - 5th decade but variable
  onset of age.
• - 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.

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• 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 structures.
• - 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.

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• Imaging and other lab studies in dominat Ataxia
• 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

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• 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 protein

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• Pathogenesis.
• CAG repeats - polyglutamine disorders (ataxin
  proteins)
• Nuclear accumulation of these proteins (normally
  in cytoplasm)
• Ataxins with gt40 glutamines toxic to the neurons.
• Ataxin1,2,3,7,atrophin
• EA1 potassium channel gene mutation on chromsome
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• EA2-calcium channel mutaton on chromosmome 19
• In some chromosomes or the loci not known

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• Autosomal Recessive Ataxia
• Most common form of inherited ataxia (50)
• 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.

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• Some of autosomal recessive ataxia
• Frederichs ataxia
• Ataxia telangectasia
• Ataxia with isolated vit E deficiency
• Abetalipoproteinemia
• ARA of Charlovox-Sanguenay

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• Friendreich's Ataxia
• Clinicla Features prevalence 2/100,000 .
• Age of onset lt25 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 many

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• ECG abnormality and HCMP- 50 pts,
• Diabetis (10-20)- insulin resistance and B cell
  dysfunction,
• skeletal and spinal deformity common. pescavus,
  pes equinovarus, scoliosis
• 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.

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• 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 frataxin.
• the exact function of ftataxin not clear- is
  mitochondrial iron availability heme synthesis.

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• 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 neoplasms.
• 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

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• Mitochondrial Ataxias.
• Each mitochondrion contains several copies of
  circular chromosomes
• mtDNA small and encodes 13 proteins component
  of respiratory chain in oxidative
  phosphorylation ATP generation
• 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 production,apoptosis
• Clinical spectrum involves cardiomyophathy and
  enchephalopathy

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• Sporadic/ Idiopathic Ataxia
• No primary cause known or no gene identified
• 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
• deficits

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• Treatments
• Most important goal in management of Pts with
  ataxia is to identify treatable disease entities
  
• Mass lesions should be ruled out and treated
  appropriately.
• 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 chemotherapy)
• A number of single case reports improvement after
  tumor removal, plasma exchange, IVIG,
  cyclophosphamide or glucocoticoids.

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• 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)

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• Avoid Exposure to metals or chemotherapy
• Gluten free diet
• Vit E therapy.
• Vit B1 and Vit B12 Supplementation in
  deficiencies
• Replace hypothyroidism.
• CSF VDRL (CNS syphilis) Rx
• Ab titer to Leigionella and Lyme- appropriate
  Antibiotics
• Surgery-thalamic stimulation for tremer and brain
  tumor
• chemotherapy and radiation for other neoplasms
• Chelating agents,hemodialysis

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• THANK YOU!!