Physiotherapy related course

1. Cerebrovascular Diseases
By Dr. Jemal S.(IMR)
5/3/2023 1

2. Outline
• Introduction
• Classification
• Risk Factors
• Signs and Symptoms
• Approach to the Patient
5/3/2023 2

3. • A stroke, or cerebrovascular accident, is
defined as an abrupt onset of a neurologic
deficit that is attributable to a focal vascular
cause.
• Thus, the definition of stroke is clinical, and
laboratory studies including brain imaging are
used to support the diagnosis
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4. • When blood flow is quickly restored, brain tissue
can recover fully and the patient’s symptoms are
only transient: this is called a transient ischemic
attack (TIA).
• The definition of TIA requires that all neurologic
signs and symptoms resolve within 24 h without
evidence of brain infarction on brain imaging.
• Stroke has occurred if the neurologic signs and
symptoms last for >24 h or brain infarction is
demonstrated
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5. 5/3/2023 5

6. • Cerebral ischemia- reduction in blood flow>
several seconds.
• symptoms manifest within seconds b/c
neurons lack glycogen, so energy failure is
rapid.
• If the cessation of flow lasts for more than a
few minutes, infarction or death of brain
tissue results
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7. • A generalized reduction in cerebral blood flow
due to systemic hypotension usually produces
syncope.
• If low cerebral blood flow persists for a longer
duration, then infarction in the border zones
between the major cerebral artery
distributions may develop
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8. Stroke – Risk Factors
• Modifiable
– Hypertension
– Tobacco use
– Hx of TIA’s
– Heart Disease
– Diabetes Mellitus
– Hypercoagulopathy
• Pregnancy, cancer, etc.
– Sickle Cell and increased RBC
– Hx of carotid Bruit
– Dyslipidemia
• Unmodifiable
–Age
–Gender
–Race
–Previous CVA
–Heredity
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9. • Ischemic
–Carotid Circulation
• Unilateral paralysis (opposite side)
• Numbness (opposite side)
• Language disturbance
– Aphasia – difficult comprehension, nonsense, difficult
reading/writing
– Dysarthria – slurred speech, abnormal pronunciation.
• Visual disturbance (opposite side)
• Monocular blindness (same side)
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10. • Ischemic
–Vertebrobasilar Circulation
• Vertigo- confused or disoriented state of mind
• Visual disturbance
– Both eyes simultaneously
• Diplopia
– Ocular palsy – inability to move to one side
– Dysconjugate gaze – asynchronous movement
• Paralysis
• Numbness
• Dysarthria
• Ataxia-loss of muscular coordination
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11. Ddx
• Differential Diagnosis of Stroke
– Head/Cervical trauma
– Meningitis/encephalitis
– Hypertensive encephalopathy
– Intracranial mass
• Tumor
• Sub/epidural hematoma
– Todd’s paralysis- a focal weakness or paralysis in a part of a
body after seizure
– Migraine
– Metabolic
• Hyper/hypo glycemia
• Post arrest ischemia
• Drug OD
--- " unmask" a prior deficit
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12. Approach to the Patient
• Rapid evaluation is essential for use of time-
sensitive treatments
• Call emergency medical services immediately
• An adequate history from an observer that no
convulsive activity occurred at the onset
reasonably excludes seizure
• Stroke mimics
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13. • . Intracranial hemorrhage is caused by
bleeding directly into or around the brain; it
produces neurologic symptoms by producing a
mass effect on neural structures, from the
toxic effects of blood itself, or by increasing
intracranial pressure.
• loss of sensory and/or motor function on one
side of the body (nearly 85% of ischemic
stroke patients have hemiparesis)
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14. • The goals in the initial phase include:
• Ensuring medical stability, with particular
attention to airway, breathing, and circulation
• Quickly reversing any conditions that are
contributing to the patient's problem
• Determining if patients with acute ischemic stroke
are candidates for thrombolytic rx
• Moving toward uncovering the pathophysiologic
basis of the patient's neurologic symptom
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15. • Patients with ICP due to hemorrhage,
vertebrobasilar ischemia can present with a
decreased respiratory drive or muscular
airway obstruction.
• Hypoventilation, with a resulting increase in
carbon dioxide, may lead to cerebral
vasodilation, which further elevates ICP
• Intubation/oxygen
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16. Hypodense area:
• Ischemic area with edema,
swelling
• Indicates >3 hours old
• No fibrinolytics!
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17. (White areas indicate
hyperdensity = blood)
Large left frontal
intracerebral hemorrhage.
Intraventricular bleeding
is also present
No fibrinolytics!
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18. Acute subarachnoid
hemorrhage
Diffuse areas of white
(hyperdense) images
Blood visible in ventricles
and multiple areas on
surface of brain
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19. Work up
• A chest x-ray, ECG, urinalysis, CBC,ESR
• serum electrolytes, blood urea nitrogen
(BUN), creatinine, blood sugar, serologic test
for syphilis, serum lipid profile,
• prothrombin time (PT), and partial
thromboplastin time (PTT) are often useful
and should be considered in all patients
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20. Management ischemic stroke
1) Medical support
(2) Intravenous thrombolytic
(3) Endovascular techniques
(4) Antithrombotic treatment
(5) Neuroprotection, and
(6) Stroke centers and rehabilitation
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21. Medical Support
• Infections
• Deep venous thrombosis (DVT) with pulmonary
embolism
• Fever
• Serum glucose
• Cerebral edema
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22. Cont…
• Blood pressure
– Collateral blood flow within the ischemic brain is blood pressure
dependent
– Blood pressure should be lowered if there is malignant hypertension
or concomitant myocardial ischemia or if blood pressure is
>185/110 mmHg and thrombolytic therapy is anticipated
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23. Thrombolytic Therapy
• Thrombolytic Agents
– showed a clear benefit for IV rtPA in selected
patients with acute stroke
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24. Antithrombotic Treatment
• Platelet Inhibition
– Aspirin is the only Antiplatelet agent that has been
proven effective for the acute treatment of ischemic
stroke
– The International Stroke Trial (IST) and the Chinese
Acute Stroke Trial (CAST) found the use of ASA
reduced
– stroke recurrence risk and mortality minimally
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25. • For primary prevention and for patients who have
experienced stroke or TIA
• Anticoagulation with warfarin reduces the risk by
about 67%, which clearly outweighs the 1% risk
per year of a major bleeding complication
• The presence of any risk factor tips the balance in
favor of anticoagulation.
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26. Neuroprotection
• Neuroprotection is the concept of providing a
treatment that prolongs the brain's tolerance to
ischemia
• Hypothermia
• Drugs that block excitatory aminoacid pathways.
• Hypothermia is a powerful neuroprotective treatment
in patients with cardiac arrest and is neuroprotective
in animal models of stroke, but it has not been
adequately studied in patients with ischemic stroke.
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27. Stroke Centers and Rehabilitation
• Improves neurologic outcome and reduces
mortality
• Occupational, physical, speech therapy
• Prevention of complications of immobility
• Physical therapy can recruit unused neural
pathways
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28. Intracranial Hemorrhage
• Hemorrhages are classified by their location
and the underlying vascular pathology
• hemorrhagic stroke
80.8 % intraparenchymal
19.2% subarachioid
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29. • Hemorrhagic Stroke
–Subarachnoid
• Aneurysm (most common)
• Arteriovenous malformation
–Intracerebral
• Hypertension (most common)
• Amyloid angiopathy in elderly
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30. 5/3/2023 30

31. C/M
• The hemorrhage generally presents as the abrupt onset of focal
neurologic deficit
• Seizures are uncommon
• Signs of increased ICP, such as headache and vomiting.
• Coma ensueThe risk for early
• neurological deterioration and the high rate of poor long-term
outcomes underscores the need for aggressive early
managements. accompanied by deep, irregular, or intermittent
respiration, a dilated and fixed ipsilateral pupil, and decerebrate
rigidity
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32. Emergency Management
• In patients presenting with a systolic BP of
150 to 220 mm Hg, acute lowering of systolic
BP to 140 mm Hg is probably safe
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33. • Stuporous or comatose patients generally are
treated presumptively for elevated ICP
–Tracheal intubation and hyperventilation
– Mannitol administration and
–Elevation of the head of the bed while surgical
consultation is obtained
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34. Poor prognosis
• extension into the ventricular system
• advanced age
• location within the posterior fossa
• depressed level of consciousness at initial
presentation
• Supratentorial hematoma >60 ml –poor
prognosis.
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35. Prevention of DVT
• Patients with ICH should have intermittent
pneumatic compression for prevention of
venous thromboembolism in addition to
elastic stockings
– (Class I;Level of Evidence: B)
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36. • After documentation of cessation of bleeding, low
dose subcutaneous low-molecular-weight heparin
or unfractionated heparin may be considered for
prevention of venous thromboembolism in
patients with lack of mobility after 1 to 4 days
from onset
• (Class IIb; Level of Evidence: B).
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37. • Hypertension is the leading cause of primary
intracerebral hemorrhage.
• Prevention is aimed at reducing hypertension,
excessive alcohol use, and use of illicit drugs
such as cocaine and amphetamines
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38. • STATINS (advice)
• In patients with a history of cerebrovascular
disease, statins clearly decrease the risk of
ischemic stroke.
• However, this beneficial effect is partly lost by
an increased risk of hemorrhagic stroke
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39. SAH
Causes
Saccular aneurysm
(80%)
Trauma
AVM
Extension from an
intraparenchymal Hg
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40. Saccular (Berry) Aneurysm
Annual risk of rupture of ASxic Aneurysm
» <1 cm -0.1 % ,
» >1 cm 0.5-1 %
» >2.5 cm (Giant )--6%
• risk factors for rupture : smoking , HTN ,
Alcohol..
• C/F : “The worst headache of my life” is
described by ~80% of patients , high index of
suspicion
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41. Complications
• Rerupture- highest in the 1st
72hrs
• Hydrocephalus : Acute, Subacute , Chronic
• Vasospasm : ischemia , @ 4- 14 days usually @
7 days
• Hyponatremia : “Cerebral Salt Wasting
Syndrome”
• Dx : Hallmark– Blood in the CSF
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42. Medical Mx
• ABC
• BP control, maintain adequate cerebral
perfusion
• Quiet room, sedation, laxatives, analgesics
• Prophylactic -phenytoin
• Antifibrinolytics – prevents rebleeding
• Statins – prevent vasospasm, decrease
mortality
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43. • ABC
• Clipping
• Craniotomy, brain retraction needed
• Coil
• Endovascular , thru femoral artery
• Less mortality and morbidity
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44. Poor prognosis
• the patient’s level of consciousness on
admission,
• age
• the amount of blood shown by initial CT
(thick subarachnoid clot and bilateral ventricular
hemorrhage)
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45. Multiple Sclerosis
• Multiple sclerosis (MS) is an autoimmune
disease of the CNS characterized by chronic
inflammation, demyelination, gliosis
(scarring), and neuronal loss; the course can
be relapsing-remitting or progressive.
• Lesions of MS typically develop at different
times and in different CNS locations (i.e., MS is
said to be disseminated in time and space).
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46. • Demyelination is the hallmark of the pathology, and
evidence of myelin degeneration is found at the
earliest time points of tissue injury.
• A remarkable feature of MS plaques is that
oligodendrocyte precursor cells survive—and in
many lesions are present in even greater numbers
than in normal tissue—but these cells fail to
differentiate into mature myelin-producing cells
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47. 5/3/2023 47

48. • MS is approximately threefold more common
in women than men.
• The age of onset is typically between 20 and
40 years (slightly later in men than in women),
but the disease can present across the
lifespan.
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49. • Well-established risk factors for MS include
–Vitamin D deficiency,
–Exposure to Epstein-Barr virus (EBV) after early
childhood, and
–Cigarette smoking
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50. C/M
• The onset of MS may be abrupt or insidious.
• Symptoms may be severe or seem so trivial
that a patient may not seek medical attention
for months or years
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51. • Exercise-induced weakness is a characteristic symptom
of MS
• The weakness is of the upper motor neuron type and
is usually accompanied by other pyramidal signs such
as spasticity, hyperreflexia, and Babinski signs
• Occasionally a tendon reflex may be lost (simulating a
lower motor neuron lesion) if an MS lesion disrupts
the afferent reflex fibers in the spinal cord
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52. • Spasticity is commonly associated with
spontaneous and movement-induced muscle
spasms.
–More than 30% of MS patients have moderate to
severe spasticity, especially in the legs
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53. • Sensory symptoms are varied and include
both paresthesias (e.g., tingling, prickling
sensations, formications, “pins and needles,”
or painful burning) and hypesthesia (e.g.,
reduced sensation, numbness, or a “dead”
feeling).
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54. Rx
• Treatment of acute attack
• Rx of progression
• Symptomatic therapy
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55. Myasthenia Gravis
• Myasthenia gravis (MG) is a neuromuscular
junction (NMJ) disorder characterized by
weakness and fatigability of skeletal muscles.
• The underlying defect is a decrease in the
number of available acetylcholine receptors
(AChRs) at NMJs due to an antibody-mediated
autoimmune attack
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56. • The cardinal features are weakness and
fatigability of muscles. The weakness
increases during repeated use (fatigue) or late
in the day and may improve following rest or
sleep.
• Overall, women are affected more frequently
than men, in a ratio of ~3:2
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57. • The diagnosis is suspected on the basis of
weakness and fatigability in the typical
distribution described above, without loss of
reflexes or impairment of sensation or other
neurologic function.
• The suspected diagnosis should always be
confirmed definitively before treatment is
undertaken
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58. Rx
• The prognosis has improved strikingly as a result
of advances in treatment. Nearly all myasthenic
patients can be returned to full productive lives
with proper therapy.
• The most useful treatments for MG include
anticholinesterase medications,
immunosuppressive agents,
thymectomy,
plasmapheresis, and
intravenous immunoglobulin (IVIg)
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59. Brain Tumors
• Brain tumors encompass neoplasms that originate in the brain
itself (primary brain tumors) or involve the brain as a metastatic
site (secondary brain tumors).
• Primary brain tumors include tumors of the brain parenchyma,
meninges, cranial nerves, and other intracranial structures (the
pituitary and pineal glands).
• Primary central nervous system lymphoma refers to non-Hodgkin
lymphoma confined to the central nervous system (CNS). The site
of origin of this type of tumor remains unknown.
• Secondary brain tumors, which originate elsewhere in the body
and metastasize to the intracranial compartment, are the most
common types of brain tumors
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60. • In children, primary CNS tumors predominate,
and about half are located in the posterior
fossa.
• In contrast, most CNS tumors in adults are
metastatic lesions to the cerebral cortex.
These differences translate to differences in
clinical presentation between pediatric and
adult malignant CNS tumors.
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61. • Gliomas, meningiomas, and embryonal
tumors account for over 95 percent of primary
intracranial neoplasms
• Gliomas account for over 80 percent of
primary CNS malignancies
• Read more on brain tumor mgt
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62. References
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63. • THANK YOU
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