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Sandesh Rayamajhi
MPT-II year
Brain tumors
๏‚ž Definition
๏‚ž Causes
๏‚ž Types
๏‚ž Clinical features
๏ƒ˜ Neurocutaneous disorders
๏‚ž Causes
๏‚ž Types
๏‚ž Clinical features
๏ƒ˜ Assessment
๏ƒ˜ PT management
๏ƒ˜
๏ƒ˜ Definition:

word โ€“ โ€œ swellingโ€
๏‚ž A tumor is commonly used as a synonym
for a neoplasm that appears enlarged in
size.
๏‚ž It is an abnormal mass of tissue which may
be solid or fluid- filled.
๏‚ž Latin
๏‚ž Genetic

factorsTransformation of normal cells to malignant
growth probably results from a variety of
different processesa)Alteration in the expression of protooncogenes
b)Inactivation of expression of tumour
suppressor genes
b) Over expression of genes controlling
growth factor
๏‚ž Cranial irradiation
๏‚ž Immunosuppression
WHO (2000)
๏‚ž based on the tissue of origin.
Neuroepithelial๏‚ž Astrocytes- Astrocytoma
๏‚ž Oligodendrocytes- Oligodendroglioma
๏‚ž Ependymal cells and choroid plexusEpendymoma
Choroid plexus papilloma
๏‚ž
๏‚ž Neurons-

Neurocytoma or ganglioglioma or
gangliocytoma
๏‚ž Pineal cells- Pineocytoma or pineoblastoma
๏‚ž Poorly differentiated and embryonal cellsMedulloblastoma
ASTROCYTOMA

OLIGODENDROGLIOMA
EPENDYMOMA

CHOROID PLEXUS
PAPILLOMA
NEUROCYTOMA

PINEOCYTOMA
MENINGIOMA

MENINGEAL SARCOMA
Meningeal melanoma
SCHWANNOMA

NEUROFIBROMA
Blood vessels
GERMINOMA

TERATOMA
CRANIOPHARYNGIOMA

PITUITARY ADENOMA
EPIDERMOID OR
DERMOID CYSTS

COLLOID CYSTS
CHORDOMA

GLOMUS JUGULARE
TUMOUR
CHONDROMA

CHONDROSARCOMA
๏‚ž Symptoms

tend to develop insidiously,
gradually progressing over a few weeks or
years, depending on the degree of malignancy.

๏‚ž Intracranial

tumours are considered in relation
to these common clinical manifestation:
๏‚ž Changes

in mental function
๏‚ž Headaches
๏‚ž Vomiting
๏‚ž Seizures- 30%
๏‚ž Periodic

bifrontal and bioccipital
headaches
๏‚ž Projectile vomiting
๏‚ž Mental torpor
๏‚ž Unsteady gait
๏‚ž Sphincteric incontinence
๏‚ž Papilledema
๏‚ž Symptoms

and signs of general cerebral
impairment and increased pressure occur
late or not at all.
๏‚ž Hereditary

disorders, characterized by
multiorgan malformations and tumours.

๏‚ž Phakomatoses

or Neurocutaneous

Syndromes
๏‚ž Disorders

of central nervous system that
additionally result in lesions on the skin
and the eye.
๏‚ž Neurofibromatosis
๏‚ž Tuberous

๏‚ž Sturge๏‚ž Von

sclerosis

Weber syndrome

Hippel- Lindau disease

๏‚ž Ataxia

Telangiectasia
๏‚ž Tuberous

sclerosis an autosomal
dominant condition.
๏‚ž Many children born with TS are the first
cases in a family.
๏‚ž Majority of TS is caused by a new gene
change (mutation).
๏‚ž Gene localized to chromosome 9 and 16.
๏‚ž NF1

is an autosomal dominant condition
๏‚ž Gene on chromosome 17.
๏‚ž NF2- autosomal dominant conditon
๏‚ž Gene on chromosome 22.
๏‚ž NF

may also be the result of a new gene
change. Half of NF cases are caused by a new
mutation.
๏‚ž Males and females are equally affected.
Schwannomatosis- a recently recognized form
of NF that is genetically distinct from NF1 and
NF2.
๏‚ž It occurs rarely.
๏‚ž The

cause of Sturge-Weber disease is
unknown and is considered to be sporadic.
๏‚ž Ataxia telangiectasia is autosomal
recessive disorder.
๏‚ž Mutation in the ATM gene- chromosome
11.
๏ƒ˜ Neurofibromatosis

(NF):
๏‚ž There are three distinct types of NF,
classified as NF I, NF II, and
Schwannomatosis.
NF1๏‚ž It is characterized by cafรฉ au lait spots and
neurofibromas.
๏‚ž Von Recklinghausenโ€™s disease.
๏‚ž Subcutaneous neurofibromata
๏‚ž Mollusca

fibrosa
๏‚ž Plexiform neuroma
Skeletal manifestations๏‚ž Scoliosis ( 50%)
๏‚ž Subperiosteal neurofibromas
๏‚ž Sphenoid wing dysplasia
๏‚ž Occular manifestations- Lisch nodules
Neurological manifestations๏‚ž Mental retardation and Epilepsy- 15%
๏‚ž Neoplasia

NF2๏‚ž It is autosomal dominant disorder
characterized by tumours of the 8th cranial
nerve ( vestibular division).
๏‚ž Cafรฉ au lait spots โ€“ rare
๏‚ž Schwannomatosis-

The primary feature is the growth of
multiple schwannomas throughout the
body except the vestibular nerve is not
involved.
๏‚ž Extremely intense pain- main symptom.
๏‚ž Numbness
๏‚ž Tingling or weakness in the fingers and
toes.
๏‚ž Autosomal

dominant disorder with high
sporadic mutation rate.
๏‚ž Characterized by cutaneous, neurologic,
renal, skeletal, cardiac and pulmonary
abnormalities.
๏‚ž Adenoma sebaceum
๏‚ž Shagreen patch.
๏‚ž Pitted teeth
๏‚ž Facial

angioma associated with a
leptomeningeal venous angioma.
๏‚ž Capillary naevus โ€“ โ€œPort wine stainโ€
๏‚ž Eye disorders
๏‚ž Atrophic hemisphere
๏‚ž Epilepsy (75% cases)
๏‚ž Hemiparesis, homonymous hemianopia
(30%)
๏‚ž Behavioral disorder and mental retardation
๏‚ž Haemangioblastomas

in the cerebellum,
spinal canal and retina and are associated
with a number of visceral pathologies:
๏‚ž Renal angioma and Renal cell carcinoma
๏‚ž Phaeochromocytoma
๏‚ž Pancreatic adenoma
๏‚ž Cysts and haemangiomas in liver and
epididymis
๏‚ž Louis-

Bar syndrome
๏‚ž Multisystem disorder is characterized by๏‚ž Cerebellar ataxia
๏‚ž Occular and cutaneous telangiectasia
๏‚ž Immunodeficiency
๏ƒ˜ Evaluation๏‚ž Comprehensive

examination and
assessment of all systems.

๏‚žA

thorough review- medical history and an
understanding of the medical diagnosis.
๏‚ž Important

psychosocial factorsoccupation, support system, personal
goals and role in the family.

๏‚ž Examination

of all the systems through
functional tasks
๏ƒ˜ Functional

Assessment๏‚ž The Functional Independence Measure
(FIM)-functional assessment tool used to
measure degree of disability, regardless of
underlying pathology and burden of care to
demonstrate functional outcomes of
rehabilitation and assist clinicians with
discharge planning.
๏ƒ˜ Goal

setting๏‚ž The functional deficits and objective
neurological findings- valuable information
to assess prognosis, establish goals, and
determine a treatment plan.
๏‚ž Maximize the potential for function,
introduce effective, task-oriented
movement strategies, and offer multiple
movement options.
๏‚ž Comprehensive

caregiver training to
independent mobility with transition back to
a work environment.
๏ƒ˜ Side

effects and Considerations๏‚ž Mindful of the side effects when developing
a plan of intervention.
๏‚ž Fatigue,

low blood count, and
gastrointestinal complaints- limit a patientโ€™s
ability to fully participate in the planned
therapy session.
๏‚ž The

clinician must be flexible to determine
the optimal time for intervention.

๏‚ž Changes

in cognition or personality as a
result of the tumourโ€™s location.
๏ƒ˜ Intervention-

๏‚ž The

ultimate goal- to achieve maximum
restoration of function, within the limits
imposed by the disease, in the clientโ€™s
preferred environment.
๏‚ž Begins in the intensive care unit and
continues in the inpatient, outpatient, and
home health settings.
๏‚ž Communication

with nursing staffregarding present medical status and an
understanding of ICP, hemodynamic
values, and monitoring devices is crucial to
determining tolerance for therapy
intervention.

.
๏‚ž Medically

stable patient- upgrade mobility
and prepare for the next stage of
rehabilitation.
๏‚ž Inpatient rehabilitation setting- Treatment
focuses on optimizing functional
capabilities to prepare for discharge.
๏‚ž Integrating

personal goals and interests
into therapeutic intervention invests the
client and family in the rehabilitation
process.
๏‚ž Prepare the client and caregivers for an
efficient transition.
๏‚ž Utilizing

motor learning principles to teach
functional mobility will best produce
transfer of learning from a constant
environment to an unpredictable home
environment.
๏‚ž Repeated

practice of specific parts of a
skill in fixed surroundings, with physical
and verbal guidance throughout the
movement, and frequent feedback during
and following the completion of the task,
are beneficial in teaching acquisition of a
specific movement or activity.
๏‚ž Practicing

the whole activity in a variable
context, with irregular feedback and
decreased physical and verbal guidance.

๏‚ž Learning

results in the ability to execute a
task in any setting.
๏‚ž Community

outings and home passes
naturally provide an environment that
facilitates learning.
๏‚ž Measure retention and transfer of learning
by the clientโ€™s performance in the
community or at home.
๏‚ž This

information- used to adjust the
treatment plan and make
recommendations for environmental
modifications that minimize physical and
cognitive demands on the client.
๏‚ž Kenneth

W. Lindsay, Ian Bone, Neurology
and Neurosurgery illustrated, 4th Ed.
๏‚ž Maurice Victor and Raymond D. Adams,
Principles of Neurology, 6th Ed.
๏‚ž Darcy A. Umphred, Neurological
Rehabilitation, 5th Ed.
๏‚ž Delisa, Physical Medicine and
Rehabilitation, 4th Ed.
๏‚ž http://www.hopkinsmedicine.org/healthlibra

ry/conditions/nervous_system_disorders/n
eurocutaneous_syndromes_85,P00794
Physiotherapy management of brain tumors and neurocutaneous disorders

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Physiotherapy management of brain tumors and neurocutaneous disorders

  • 2. Brain tumors ๏‚ž Definition ๏‚ž Causes ๏‚ž Types ๏‚ž Clinical features ๏ƒ˜ Neurocutaneous disorders ๏‚ž Causes ๏‚ž Types ๏‚ž Clinical features ๏ƒ˜ Assessment ๏ƒ˜ PT management ๏ƒ˜
  • 3. ๏ƒ˜ Definition: word โ€“ โ€œ swellingโ€ ๏‚ž A tumor is commonly used as a synonym for a neoplasm that appears enlarged in size. ๏‚ž It is an abnormal mass of tissue which may be solid or fluid- filled. ๏‚ž Latin
  • 4. ๏‚ž Genetic factorsTransformation of normal cells to malignant growth probably results from a variety of different processesa)Alteration in the expression of protooncogenes b)Inactivation of expression of tumour suppressor genes
  • 5. b) Over expression of genes controlling growth factor ๏‚ž Cranial irradiation ๏‚ž Immunosuppression
  • 6. WHO (2000) ๏‚ž based on the tissue of origin. Neuroepithelial๏‚ž Astrocytes- Astrocytoma ๏‚ž Oligodendrocytes- Oligodendroglioma ๏‚ž Ependymal cells and choroid plexusEpendymoma Choroid plexus papilloma ๏‚ž
  • 7. ๏‚ž Neurons- Neurocytoma or ganglioglioma or gangliocytoma ๏‚ž Pineal cells- Pineocytoma or pineoblastoma ๏‚ž Poorly differentiated and embryonal cellsMedulloblastoma
  • 11.
  • 21.
  • 22. ๏‚ž Symptoms tend to develop insidiously, gradually progressing over a few weeks or years, depending on the degree of malignancy. ๏‚ž Intracranial tumours are considered in relation to these common clinical manifestation:
  • 23. ๏‚ž Changes in mental function ๏‚ž Headaches ๏‚ž Vomiting ๏‚ž Seizures- 30%
  • 24. ๏‚ž Periodic bifrontal and bioccipital headaches ๏‚ž Projectile vomiting ๏‚ž Mental torpor ๏‚ž Unsteady gait ๏‚ž Sphincteric incontinence ๏‚ž Papilledema
  • 25. ๏‚ž Symptoms and signs of general cerebral impairment and increased pressure occur late or not at all.
  • 26. ๏‚ž Hereditary disorders, characterized by multiorgan malformations and tumours. ๏‚ž Phakomatoses or Neurocutaneous Syndromes ๏‚ž Disorders of central nervous system that additionally result in lesions on the skin and the eye.
  • 27. ๏‚ž Neurofibromatosis ๏‚ž Tuberous ๏‚ž Sturge๏‚ž Von sclerosis Weber syndrome Hippel- Lindau disease ๏‚ž Ataxia Telangiectasia
  • 28. ๏‚ž Tuberous sclerosis an autosomal dominant condition. ๏‚ž Many children born with TS are the first cases in a family. ๏‚ž Majority of TS is caused by a new gene change (mutation). ๏‚ž Gene localized to chromosome 9 and 16.
  • 29. ๏‚ž NF1 is an autosomal dominant condition ๏‚ž Gene on chromosome 17. ๏‚ž NF2- autosomal dominant conditon ๏‚ž Gene on chromosome 22.
  • 30. ๏‚ž NF may also be the result of a new gene change. Half of NF cases are caused by a new mutation. ๏‚ž Males and females are equally affected. Schwannomatosis- a recently recognized form of NF that is genetically distinct from NF1 and NF2. ๏‚ž It occurs rarely.
  • 31. ๏‚ž The cause of Sturge-Weber disease is unknown and is considered to be sporadic. ๏‚ž Ataxia telangiectasia is autosomal recessive disorder. ๏‚ž Mutation in the ATM gene- chromosome 11.
  • 32. ๏ƒ˜ Neurofibromatosis (NF): ๏‚ž There are three distinct types of NF, classified as NF I, NF II, and Schwannomatosis. NF1๏‚ž It is characterized by cafรฉ au lait spots and neurofibromas. ๏‚ž Von Recklinghausenโ€™s disease. ๏‚ž Subcutaneous neurofibromata
  • 33. ๏‚ž Mollusca fibrosa ๏‚ž Plexiform neuroma Skeletal manifestations๏‚ž Scoliosis ( 50%) ๏‚ž Subperiosteal neurofibromas ๏‚ž Sphenoid wing dysplasia ๏‚ž Occular manifestations- Lisch nodules
  • 34. Neurological manifestations๏‚ž Mental retardation and Epilepsy- 15% ๏‚ž Neoplasia NF2๏‚ž It is autosomal dominant disorder characterized by tumours of the 8th cranial nerve ( vestibular division). ๏‚ž Cafรฉ au lait spots โ€“ rare
  • 35. ๏‚ž Schwannomatosis- The primary feature is the growth of multiple schwannomas throughout the body except the vestibular nerve is not involved. ๏‚ž Extremely intense pain- main symptom. ๏‚ž Numbness ๏‚ž Tingling or weakness in the fingers and toes.
  • 36.
  • 37.
  • 38. ๏‚ž Autosomal dominant disorder with high sporadic mutation rate. ๏‚ž Characterized by cutaneous, neurologic, renal, skeletal, cardiac and pulmonary abnormalities. ๏‚ž Adenoma sebaceum ๏‚ž Shagreen patch. ๏‚ž Pitted teeth
  • 39.
  • 40. ๏‚ž Facial angioma associated with a leptomeningeal venous angioma. ๏‚ž Capillary naevus โ€“ โ€œPort wine stainโ€ ๏‚ž Eye disorders ๏‚ž Atrophic hemisphere ๏‚ž Epilepsy (75% cases) ๏‚ž Hemiparesis, homonymous hemianopia (30%) ๏‚ž Behavioral disorder and mental retardation
  • 41.
  • 42. ๏‚ž Haemangioblastomas in the cerebellum, spinal canal and retina and are associated with a number of visceral pathologies: ๏‚ž Renal angioma and Renal cell carcinoma ๏‚ž Phaeochromocytoma ๏‚ž Pancreatic adenoma ๏‚ž Cysts and haemangiomas in liver and epididymis
  • 43.
  • 44. ๏‚ž Louis- Bar syndrome ๏‚ž Multisystem disorder is characterized by๏‚ž Cerebellar ataxia ๏‚ž Occular and cutaneous telangiectasia ๏‚ž Immunodeficiency
  • 45.
  • 46. ๏ƒ˜ Evaluation๏‚ž Comprehensive examination and assessment of all systems. ๏‚žA thorough review- medical history and an understanding of the medical diagnosis.
  • 47. ๏‚ž Important psychosocial factorsoccupation, support system, personal goals and role in the family. ๏‚ž Examination of all the systems through functional tasks
  • 48. ๏ƒ˜ Functional Assessment๏‚ž The Functional Independence Measure (FIM)-functional assessment tool used to measure degree of disability, regardless of underlying pathology and burden of care to demonstrate functional outcomes of rehabilitation and assist clinicians with discharge planning.
  • 49. ๏ƒ˜ Goal setting๏‚ž The functional deficits and objective neurological findings- valuable information to assess prognosis, establish goals, and determine a treatment plan. ๏‚ž Maximize the potential for function, introduce effective, task-oriented movement strategies, and offer multiple movement options.
  • 50. ๏‚ž Comprehensive caregiver training to independent mobility with transition back to a work environment.
  • 51. ๏ƒ˜ Side effects and Considerations๏‚ž Mindful of the side effects when developing a plan of intervention. ๏‚ž Fatigue, low blood count, and gastrointestinal complaints- limit a patientโ€™s ability to fully participate in the planned therapy session.
  • 52. ๏‚ž The clinician must be flexible to determine the optimal time for intervention. ๏‚ž Changes in cognition or personality as a result of the tumourโ€™s location.
  • 53. ๏ƒ˜ Intervention- ๏‚ž The ultimate goal- to achieve maximum restoration of function, within the limits imposed by the disease, in the clientโ€™s preferred environment. ๏‚ž Begins in the intensive care unit and continues in the inpatient, outpatient, and home health settings.
  • 54. ๏‚ž Communication with nursing staffregarding present medical status and an understanding of ICP, hemodynamic values, and monitoring devices is crucial to determining tolerance for therapy intervention. .
  • 55. ๏‚ž Medically stable patient- upgrade mobility and prepare for the next stage of rehabilitation. ๏‚ž Inpatient rehabilitation setting- Treatment focuses on optimizing functional capabilities to prepare for discharge.
  • 56. ๏‚ž Integrating personal goals and interests into therapeutic intervention invests the client and family in the rehabilitation process. ๏‚ž Prepare the client and caregivers for an efficient transition.
  • 57. ๏‚ž Utilizing motor learning principles to teach functional mobility will best produce transfer of learning from a constant environment to an unpredictable home environment.
  • 58. ๏‚ž Repeated practice of specific parts of a skill in fixed surroundings, with physical and verbal guidance throughout the movement, and frequent feedback during and following the completion of the task, are beneficial in teaching acquisition of a specific movement or activity.
  • 59. ๏‚ž Practicing the whole activity in a variable context, with irregular feedback and decreased physical and verbal guidance. ๏‚ž Learning results in the ability to execute a task in any setting.
  • 60. ๏‚ž Community outings and home passes naturally provide an environment that facilitates learning. ๏‚ž Measure retention and transfer of learning by the clientโ€™s performance in the community or at home.
  • 61. ๏‚ž This information- used to adjust the treatment plan and make recommendations for environmental modifications that minimize physical and cognitive demands on the client.
  • 62. ๏‚ž Kenneth W. Lindsay, Ian Bone, Neurology and Neurosurgery illustrated, 4th Ed. ๏‚ž Maurice Victor and Raymond D. Adams, Principles of Neurology, 6th Ed. ๏‚ž Darcy A. Umphred, Neurological Rehabilitation, 5th Ed. ๏‚ž Delisa, Physical Medicine and Rehabilitation, 4th Ed.