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Ishcemic and HemorrhagicIshcemic and Hemorrhagic
stroke - A light onstroke - A light on
Integrated approachIntegrated approach
ByBy
Dr Jayagovinda UkkinadkaDr Jayagovinda Ukkinadka
““Ukkinadkas Ayurveda”Ukkinadkas Ayurveda”
Stroke
 Stroke is characterized by the sudden
loss of blood circulation to an area of the
brain, resulting in a corresponding loss of
neurological function.
 Stroke is a nonspecific term
encompassing a heterogeneous group of
pathophysiologic causes.
In Ayurveda, in Simple words
Samanavritha Vyanavayu
Stroke can be explained as Samanavritha
Vyanavayu.
Here The brain centers responsible for body
movement (regulated by vyanavayu) is
affected by obstructed peripheral blood
circulation (regulated by Smanavayu)
Various etiological factors which in turn
produces Srothorodha or Srothobheda (in
Murdhni) causes this condition.
Consider Avarana of other vatha
factors also
Samana vayu Avarana of Prana vayu,
Udana vayu and Apana vayu should also
be considered depending upon the signs
and symptoms involved.
Samanavritha Vyanavayu
Lakshana And Chikitsa
• Murcha, Tandra, Pralapa, Angasada, Agni,
Oja and Bala kshaya.
• Treatment is Vyayama and Laghu bhojana
along with other Vathavyadhi chikitsa.
• Also consider chikitsa of Avaraka followed
by Avritha depending upon the
pathophysiology.
Ishchemic & Hemorhagic stroke
Broadly stroke is classified into two.
 Ischemic &
 Hemorhagic
Ischemic stroke- 3 major types
 Large artery infarction
 Small-vessel, or lacunar infarction
 Cardioembolic infarction
Others are
 Thrombotic stroke
 Water shed infarcts
Non modifiable Risk factors
 Age
 Race
 Sex
 History of migraine headaches
 Sickle cell disease
 Fibromuscular dysplasia
 Heredity
Modifiable risk factors
 Hypertension (the most important)
 Diabetes mellitus
 Cardiac disease
 Hypercholesterolemia
 Transient ischemic attacks (TIAs)
 Carotid stenosis
 Hyper homocystinemia
 Lifestyle issues - Excessive alcohol intake, tobacco use,
illicit drug use, obesity, physical inactivity
 Oral contraceptive use
ACA-MCA-PCA territory
Large artery infarct-MCA left side
Middle cerebral artery
stroke
 Contralateral hemiparesis & hypesthesia,
 Ipsilateral hemianopia, & gaze preference
toward the side of the lesion.
 Agnosia is common (sensory damage)
 Aphasia - if the lesion occurs in the dominant
hemisphere.
 Since the MCA supplies the upper extremity
motor strip, weakness of the arm and face is
usually worse than that of the lower limb.
Anterior cerebral artery
stroke
 ACA occlusions primarily affect frontal lobe
function
 can result in disinhibition and speech
perseveration, producing primitive reflexes (eg,
grasping, sucking reflexes)
 altered mental status, impaired judgment
 contralateral weakness (greater in legs
than arms), contralateral cortical sensory
deficits gait apraxia, and urinary incontinence.
Posterior cerebral artery
stroke
 Affect vision and thought
 producing contralateral homonymous
hemianopia, cortical blindness, visual
agnosia, altered mental status, and
impaired memory.
 Other features include
Posterior cerebral artery
stroke
 Vertigo
 Nystagmus
 Diplopia
 Visual field deficits
 Dysphagia
 Dysarthria
 Facial hypesthesia
 Syncope
 Ataxia
MCA and ACA infarct with
petechial hemorhage
Internal Carotid artery
occlusion
Lacunar infarct – in CT and MRI
 Infarct diameter less than 1.5 cm
 Due to occlusion in circle of willis either in MCA
or ACA territory
Internal capsule - thalamus
 1, Insula. 2, Internal capsule. 3, Caudate
nucleus. 4, Putamen. 5, Posterior limb, internal
capsule. 6, Splenium, corpus callosum.7, Thalamus.
Investigation modalities
 CBC
 Blood Chemical analysis
 CT scan
 MRI
 MRA
 ECG, Echo cardiography etc as
necessary
ISCHEMIC CORE
 An acute vascular occlusion produces
heterogeneous regions of ischemia in the
affected vascular territory. The quantity of local
blood flow is made up of any residual flow in
the major arterial source and the collateral
supply, if any.
 Regions of the brain with CBF lower than 10
mL/100g of tissue/min are referred to
collectively as the core, and these cells are
presumed to die within minutes of stroke
onset.
PENUMBRA
 Zones of decreased or marginal
perfusion (CBF < 25 mL/100g of
tissue/min) are collectively called the
ischemic penumbra. Tissue in the
penumbra can remain viable for several
hours because of marginal tissue
perfusion.
Saving Penumbra
 In Acute ischemic stroke the current modern
approach is to save and to convert penumbra to
normal tissues as much as possible
 Thrombolytic therapy is the recent addition, others
are use of antiplatelet and anti coagulant drugs to
prevent the recurrence of stroke.
The main aim of the medication in
modern medicine are
 Thrombolytic-alteplase (rt-PA)
 Reperfusion-recanalisation
 Antiplatelet- Clopidogrel, aspirin
 Anticoagulants-warfarin etc- usually in
thromboembolic stroke
 Neuroprotective- citicoline, vitamins etc
 Symptomatic management
Major drugs used in modern
medicine
 Thrombolytic
 Antiplatelet and anti coagulants
 Antipyretic drugs
 Anti hypertensives
 Diuretics to reduce cerebral edema
 Anti epileptics in case of seizure
 And all symptomatic approach to handle the
different situation
Management of Hypertension in
Ischemic stroke
 Sudden bringing down of blood pressure
is not recommended in ischemic stroke
 BP <200/120 should not be managed
aggressively and should wait for
spontaneous recovery. But BP above this
should be treated but care should be
taken so that sudden fall in BP should be
avoided to prevent fall in blood perfusion
Main aim of Treatment in UA
 Reperfusion- Theekshna Nasya (TN)
 Antiplatelet- Cholestonorm Capsule
 Neuroprotective- Herbal preparations
 Protecting vitals-symptomatic management
 Encouraging Neuroplasticity- by
1. TN, Irritant Lepas, Pindasweda,
Physiotherapy & Accupunture
2. Internal medicines to encourage possible
regeneration
Theekshna Nasya (TN)
 TN is the 1st
treatment to be considered
in Management of Acute CVA. But
should be very cautious before
administration.
 This simultaneously treats Avaraka and
Avritha.
TN Indication in Acute CVA
 Ischemic CVA
 Ischemic CVA with BP <190/110
 Ischemic CVA with hypotension- an ideal
treatment
TN can be used with Caution in
 All Acute Hemorhagic CVA without headache,
vomitting and siezure
 Acute Hemorhagic CVA with BP <190/110
 CVA with Bulbar Palsy
 Acute Ischemic or Hemorhagic CVA who is
comatose/stupor with Bulbar Palsy
 CVA ischemic with BP >190/110 and <220/120
TN is Contra indicated in Acute
CVA in the following condns.
 Hemorrhagic stroke with seizure, neck
stiffness, headache and vomiting till
stabilisation.
 Hemorrhagic stroke with BP> 190/110
 Massive hemorhagic stroke- 1st
2-4 days
 Large artery infarct with BP >220/120
 CVA in a patient with h/o epilepsy.
 In Huge ischemic stroke, who is already
under anti coagulants with INR >3 IU or high
doses of anti platelets.
TN Ingredients
Mode of Action of TN in Acute
CVA- A hypothesis
Perfusion
 Immediately after administration of TN BP
raises to its peak up to 220-280/130-170 mm
of Hg in most of the patients and gradually
comes down to mid phase in 20-30 minutes
and previous level in 1-6 hours depending
upon the persistance of irritation, in some
patients constantly maintained in high mid
level for some hours.
Mode of Action of TN in Acute
CVA- a hypothesis
 Perfusion
This sudden hike in blood pressure helps
in flushing of blood to the Penumbra
area and also encourages fast collateral
circulation to reach penumbra and can
save the dying brain tissue.
Mode of Action of TN in Acute &
Chronic CVA - A hypothesis
 Neuroplasticity
Neuroplasticity is activation of the spared
adjacent latent neurons which are
capable of doing the functions of
damaged cells. If such cells are viable
action of TN is excellent.
Complications of TN
 Hemorrhagic conversion of Ischemic
stroke
 worsening of hemorrhagic stroke
 Increase in the Intracranial pressure which
may ultimately result in reduced perfusion.
(Repeated intermittent administration
must be avoided)
 Possibility of development of aspiration
pneumonia in comatose pts especially
with Bulbar palsy.
Mode of Action of Irritant Lepas
 Neuroplasticity by stimulating the CNS
through nerve endings
 Possibility of absorption of active lipid
soluble molecules through skin having
specific neuroprotective activity
Lepas
 Saindhavadi Lepa- Saindhava,
Grihadhooma and Gingelly Oil
 Agni chikitsa Lepa
Pinda sweda
 Oil massage with specific herbal oil
which may also contain some specific
neuroprotective molecules.
 Massage and phomentation once again
stimulates CNS through Nerve endings
which encourages neuroplasticity.
Pindasweda Usually practiced
 Shastikashali Pindasweda
 Masha Pindasweda
Others
 Pizichil
 Annalepana
Main oils used are
Mahamasha taila and Agni taila (prop)
Shirodhara
 Which helps to subside anxiety,
depression, and psychological symptoms
which is very common in CVA
 Also helps in gradual reduction of
hypertension
 Commonly practiced are Taila and Takra
dhara
Basti
 We also treat some patients with
medicated enema if found essential
Accupuncture & Physiotherapy
 Stimulates Nerve endings and helps in
neuroplasticity
 Rehabilitation through Physiotherapy.
 We use a special technique of inducing
pressure over pain points a variety of
Marma therapy – Ayurveda
physiotherapy.
Herbal medicines
 Cholestonorm Capsule in ischemic stroke
 Main ingredients are garlic, Ajwain, Krishna
jeeraka, Saindhava lavana, Shunti, and
Chandraprabha vati with additional shilajithu.
 Main action as antiplatlet drug. Confirmed the
action by observing the bleeding and clotting
time. Also helpful in reducing Cholesterol and
Triglyceride level.
Kwatha preparations
 Mashathmagupthadi kwatha
 Balakulathadi kwatha
 Dhanadanayanadi kwatha
 Bala godhumadi kwatha
 Rasna sapthaka kwatha
 Bala jeerakadi kwatha etc
Considering the associated symptoms
Kapikachu and Ashwagandha
churna
 5g three times daily as a neuroprotective
and to improve healing power.
 Kapikachu alone - specially we use in
cerebellar stroke with gait ataxia gives
tremendous result. Dosage must be 15-
25g per day in 3-5 divided doses.
Projeny M tablet
 Improved version of Pusphadhanva Ras
where we reduced the Naga bhasma to
1/10th
and added with Jasada bhasma
and trace of Swarna bhasma.
 Improves healing ability of the tissues,
and used as neuroprotective
Kshirabala Avarthitha
 As a rejuvenative drug, and as anupana
with Mashathmaguptha kwatha
Nasika Taila (prop)
 TN can not be used for long time.
 Hence in chronic management, Nasya
which is not a Marsha nor Prathimarsha
but with mid potency which can be used
for long time without any complicaton, we
use Nasika taila to encourage
neuroplasticity.
 Main ingredients are Kokilaksha beeja,
Hingu and Gomuthra
Thank You

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Ishcemic and hemorrhagic stroke, a light on integrated approach

  • 1. Ishcemic and HemorrhagicIshcemic and Hemorrhagic stroke - A light onstroke - A light on Integrated approachIntegrated approach ByBy Dr Jayagovinda UkkinadkaDr Jayagovinda Ukkinadka ““Ukkinadkas Ayurveda”Ukkinadkas Ayurveda”
  • 2. Stroke  Stroke is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurological function.  Stroke is a nonspecific term encompassing a heterogeneous group of pathophysiologic causes.
  • 3. In Ayurveda, in Simple words Samanavritha Vyanavayu Stroke can be explained as Samanavritha Vyanavayu. Here The brain centers responsible for body movement (regulated by vyanavayu) is affected by obstructed peripheral blood circulation (regulated by Smanavayu) Various etiological factors which in turn produces Srothorodha or Srothobheda (in Murdhni) causes this condition.
  • 4. Consider Avarana of other vatha factors also Samana vayu Avarana of Prana vayu, Udana vayu and Apana vayu should also be considered depending upon the signs and symptoms involved.
  • 5. Samanavritha Vyanavayu Lakshana And Chikitsa • Murcha, Tandra, Pralapa, Angasada, Agni, Oja and Bala kshaya. • Treatment is Vyayama and Laghu bhojana along with other Vathavyadhi chikitsa. • Also consider chikitsa of Avaraka followed by Avritha depending upon the pathophysiology.
  • 6. Ishchemic & Hemorhagic stroke Broadly stroke is classified into two.  Ischemic &  Hemorhagic
  • 7. Ischemic stroke- 3 major types  Large artery infarction  Small-vessel, or lacunar infarction  Cardioembolic infarction Others are  Thrombotic stroke  Water shed infarcts
  • 8. Non modifiable Risk factors  Age  Race  Sex  History of migraine headaches  Sickle cell disease  Fibromuscular dysplasia  Heredity
  • 9. Modifiable risk factors  Hypertension (the most important)  Diabetes mellitus  Cardiac disease  Hypercholesterolemia  Transient ischemic attacks (TIAs)  Carotid stenosis  Hyper homocystinemia  Lifestyle issues - Excessive alcohol intake, tobacco use, illicit drug use, obesity, physical inactivity  Oral contraceptive use
  • 10.
  • 11.
  • 14. Middle cerebral artery stroke  Contralateral hemiparesis & hypesthesia,  Ipsilateral hemianopia, & gaze preference toward the side of the lesion.  Agnosia is common (sensory damage)  Aphasia - if the lesion occurs in the dominant hemisphere.  Since the MCA supplies the upper extremity motor strip, weakness of the arm and face is usually worse than that of the lower limb.
  • 15. Anterior cerebral artery stroke  ACA occlusions primarily affect frontal lobe function  can result in disinhibition and speech perseveration, producing primitive reflexes (eg, grasping, sucking reflexes)  altered mental status, impaired judgment  contralateral weakness (greater in legs than arms), contralateral cortical sensory deficits gait apraxia, and urinary incontinence.
  • 16. Posterior cerebral artery stroke  Affect vision and thought  producing contralateral homonymous hemianopia, cortical blindness, visual agnosia, altered mental status, and impaired memory.  Other features include
  • 17. Posterior cerebral artery stroke  Vertigo  Nystagmus  Diplopia  Visual field deficits  Dysphagia  Dysarthria  Facial hypesthesia  Syncope  Ataxia
  • 18. MCA and ACA infarct with petechial hemorhage
  • 20. Lacunar infarct – in CT and MRI  Infarct diameter less than 1.5 cm  Due to occlusion in circle of willis either in MCA or ACA territory
  • 21. Internal capsule - thalamus  1, Insula. 2, Internal capsule. 3, Caudate nucleus. 4, Putamen. 5, Posterior limb, internal capsule. 6, Splenium, corpus callosum.7, Thalamus.
  • 22. Investigation modalities  CBC  Blood Chemical analysis  CT scan  MRI  MRA  ECG, Echo cardiography etc as necessary
  • 23. ISCHEMIC CORE  An acute vascular occlusion produces heterogeneous regions of ischemia in the affected vascular territory. The quantity of local blood flow is made up of any residual flow in the major arterial source and the collateral supply, if any.  Regions of the brain with CBF lower than 10 mL/100g of tissue/min are referred to collectively as the core, and these cells are presumed to die within minutes of stroke onset.
  • 24. PENUMBRA  Zones of decreased or marginal perfusion (CBF < 25 mL/100g of tissue/min) are collectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion.
  • 25. Saving Penumbra  In Acute ischemic stroke the current modern approach is to save and to convert penumbra to normal tissues as much as possible  Thrombolytic therapy is the recent addition, others are use of antiplatelet and anti coagulant drugs to prevent the recurrence of stroke.
  • 26.
  • 27. The main aim of the medication in modern medicine are  Thrombolytic-alteplase (rt-PA)  Reperfusion-recanalisation  Antiplatelet- Clopidogrel, aspirin  Anticoagulants-warfarin etc- usually in thromboembolic stroke  Neuroprotective- citicoline, vitamins etc  Symptomatic management
  • 28. Major drugs used in modern medicine  Thrombolytic  Antiplatelet and anti coagulants  Antipyretic drugs  Anti hypertensives  Diuretics to reduce cerebral edema  Anti epileptics in case of seizure  And all symptomatic approach to handle the different situation
  • 29. Management of Hypertension in Ischemic stroke  Sudden bringing down of blood pressure is not recommended in ischemic stroke  BP <200/120 should not be managed aggressively and should wait for spontaneous recovery. But BP above this should be treated but care should be taken so that sudden fall in BP should be avoided to prevent fall in blood perfusion
  • 30. Main aim of Treatment in UA  Reperfusion- Theekshna Nasya (TN)  Antiplatelet- Cholestonorm Capsule  Neuroprotective- Herbal preparations  Protecting vitals-symptomatic management  Encouraging Neuroplasticity- by 1. TN, Irritant Lepas, Pindasweda, Physiotherapy & Accupunture 2. Internal medicines to encourage possible regeneration
  • 31. Theekshna Nasya (TN)  TN is the 1st treatment to be considered in Management of Acute CVA. But should be very cautious before administration.  This simultaneously treats Avaraka and Avritha.
  • 32. TN Indication in Acute CVA  Ischemic CVA  Ischemic CVA with BP <190/110  Ischemic CVA with hypotension- an ideal treatment
  • 33. TN can be used with Caution in  All Acute Hemorhagic CVA without headache, vomitting and siezure  Acute Hemorhagic CVA with BP <190/110  CVA with Bulbar Palsy  Acute Ischemic or Hemorhagic CVA who is comatose/stupor with Bulbar Palsy  CVA ischemic with BP >190/110 and <220/120
  • 34. TN is Contra indicated in Acute CVA in the following condns.  Hemorrhagic stroke with seizure, neck stiffness, headache and vomiting till stabilisation.  Hemorrhagic stroke with BP> 190/110  Massive hemorhagic stroke- 1st 2-4 days  Large artery infarct with BP >220/120  CVA in a patient with h/o epilepsy.  In Huge ischemic stroke, who is already under anti coagulants with INR >3 IU or high doses of anti platelets.
  • 36. Mode of Action of TN in Acute CVA- A hypothesis Perfusion  Immediately after administration of TN BP raises to its peak up to 220-280/130-170 mm of Hg in most of the patients and gradually comes down to mid phase in 20-30 minutes and previous level in 1-6 hours depending upon the persistance of irritation, in some patients constantly maintained in high mid level for some hours.
  • 37. Mode of Action of TN in Acute CVA- a hypothesis  Perfusion This sudden hike in blood pressure helps in flushing of blood to the Penumbra area and also encourages fast collateral circulation to reach penumbra and can save the dying brain tissue.
  • 38. Mode of Action of TN in Acute & Chronic CVA - A hypothesis  Neuroplasticity Neuroplasticity is activation of the spared adjacent latent neurons which are capable of doing the functions of damaged cells. If such cells are viable action of TN is excellent.
  • 39. Complications of TN  Hemorrhagic conversion of Ischemic stroke  worsening of hemorrhagic stroke  Increase in the Intracranial pressure which may ultimately result in reduced perfusion. (Repeated intermittent administration must be avoided)  Possibility of development of aspiration pneumonia in comatose pts especially with Bulbar palsy.
  • 40. Mode of Action of Irritant Lepas  Neuroplasticity by stimulating the CNS through nerve endings  Possibility of absorption of active lipid soluble molecules through skin having specific neuroprotective activity
  • 41. Lepas  Saindhavadi Lepa- Saindhava, Grihadhooma and Gingelly Oil  Agni chikitsa Lepa
  • 42. Pinda sweda  Oil massage with specific herbal oil which may also contain some specific neuroprotective molecules.  Massage and phomentation once again stimulates CNS through Nerve endings which encourages neuroplasticity.
  • 43. Pindasweda Usually practiced  Shastikashali Pindasweda  Masha Pindasweda Others  Pizichil  Annalepana Main oils used are Mahamasha taila and Agni taila (prop)
  • 44. Shirodhara  Which helps to subside anxiety, depression, and psychological symptoms which is very common in CVA  Also helps in gradual reduction of hypertension  Commonly practiced are Taila and Takra dhara
  • 45. Basti  We also treat some patients with medicated enema if found essential
  • 46. Accupuncture & Physiotherapy  Stimulates Nerve endings and helps in neuroplasticity  Rehabilitation through Physiotherapy.  We use a special technique of inducing pressure over pain points a variety of Marma therapy – Ayurveda physiotherapy.
  • 47. Herbal medicines  Cholestonorm Capsule in ischemic stroke  Main ingredients are garlic, Ajwain, Krishna jeeraka, Saindhava lavana, Shunti, and Chandraprabha vati with additional shilajithu.  Main action as antiplatlet drug. Confirmed the action by observing the bleeding and clotting time. Also helpful in reducing Cholesterol and Triglyceride level.
  • 48. Kwatha preparations  Mashathmagupthadi kwatha  Balakulathadi kwatha  Dhanadanayanadi kwatha  Bala godhumadi kwatha  Rasna sapthaka kwatha  Bala jeerakadi kwatha etc Considering the associated symptoms
  • 49. Kapikachu and Ashwagandha churna  5g three times daily as a neuroprotective and to improve healing power.  Kapikachu alone - specially we use in cerebellar stroke with gait ataxia gives tremendous result. Dosage must be 15- 25g per day in 3-5 divided doses.
  • 50. Projeny M tablet  Improved version of Pusphadhanva Ras where we reduced the Naga bhasma to 1/10th and added with Jasada bhasma and trace of Swarna bhasma.  Improves healing ability of the tissues, and used as neuroprotective
  • 51. Kshirabala Avarthitha  As a rejuvenative drug, and as anupana with Mashathmaguptha kwatha
  • 52. Nasika Taila (prop)  TN can not be used for long time.  Hence in chronic management, Nasya which is not a Marsha nor Prathimarsha but with mid potency which can be used for long time without any complicaton, we use Nasika taila to encourage neuroplasticity.  Main ingredients are Kokilaksha beeja, Hingu and Gomuthra