Stroke presentation with unani concept

1. 1
S
T
R
O
K
E
Presented By:
Zoheb Alam Khan
Dept. Of IBT
Under kind supervision of:
Dr. Abdul Nasir Ansari
HoD,Dept. Of IBT

2. 2
S
T
R
O
K
E
Presented By:
Zoheb Alam Khan
Dept. Of IBT
Under kind supervision of:
Dr. Abdul Nasir Ansari
HoD, Dept. Of IBT

3. 3
Stroke
• A stroke is a medical emergency in which the blood supply to
any portion of the brain is interrupted or reduced.
• Definition
Stroke
• Clinical syndrome of rapid onset of focal deficits of brain
function lasting more than 24 hours or leading to death (WHO)
Ischemic attack (TIA)
• Clinical syndrome of rapid onset of focal deficits of brain
function which resolves within 24 hours
• Alternative names: Cerebrovascular accident/ disease (CVA),
Cerebral infarction, Cerebral hemorrhage, Brain Attack

4. 4
Principle Brain Arteries

5. 5
Blood Supply of Brain
 Internal Carotid Arteries :transfer oxygenated blood from the
common carotid arteries of the neck to the circle of Willis.
 Circle of Willis :transfers oxygenated blood from incoming
arteries to deep internal arteries of the brain.
 Vertebral Arteries : transfer oxygenated blood from the
subclavian arteries, up through the transverse foraminae of the
cervical vertebrae and to the basilar artery of the brain.
 Basilar Artery : transfers oxygenated blood from the vertebral
arteries to the circle of Willis of thebrain.

6. 6
Epidemiology
 Stroke is the third most common cause of death in high-
income countries after cancers and ischaemic heart disease,
and the most common cause of severe physical disability.
 Stroke is the second leading cause of death for people above
the age of 60 years, and the fifth leading cause in people
aged 15 to 59 years old.
 Every year 20 million people suffer from stroke out which
5.7 millon die of it.
 The estimated age- adjusted prevalence rate for stroke in
India is 84/100,000 and 262/100,000 in rural and between
334/100,000 and 424/100,000 in urban area.

7. 7
Clinical classification of stroke
TIA (Transient ischemic attack ):
• The standard definition of TIA requires that all neurologic signs
and symptoms resolve within 24 hrs regardless of whether there
is imaging evidence of new permanent brain injury.
Stroke:
• The term stroke is reserved for those events in which symptoms
last more than 24 hours.
Progressing stroke (or stroke in evolution):
• This describes a stroke in which the focal neurological deficit
worsens after the patient first presents. Such worsening may be
due to increasing volume of infarction, haemorrhage or related
oedema.
Completed stroke :
This describes a stroke in which the focal deficit persists and is not
progressing.

8. 8
Types of stroke:

9. 9
Ischemic Stroke:
• A blood vessel becomes
blocked and the blood
supply to that part of your
brain is blocked.
• 80% of strokes
• Types of Ischemic strokes:
– Thrombotic Stroke
– Embolic Stroke

10. 10
Etiology of Ischemic stroke
Thrombotic
Lacunar stroke
Large vessel thrombosis
Hypercoagulable disorders
Embolic
Artery to artery
Carotid bifurcation
Aortic arch
Cardioembolic
Atrial fibrillation
Myocardial infarction
Mural thrombus
Bacterial endocarditis
Mitral stenosis
Paradoxical embolus

11. 11
Thrombotic Stroke
• Atherosclerosis is the most common pathology leading to
thrombotic occlusion of blood vessels
• Hypercoagulable disorders – uncommon cause
– Antiphospholipid syndrome
– Sickle cell anemia
– Polycythemia vera
– Homocysteinemia
• Vasculitis: PAN, Wegener’s granulomatosis, giant cell arteritis
• Lacunar stroke
• Accounts for 20% of all strokes
• Results from occlusion of small deep penetrating arteries of the
brain
• Pathology: lipohyalinosis & microatheroma
• Thrombosis leads to small infarcts known as lacunes
• Clinically manifested as lacunar syndromes

12. 12
Embolic Stroke
Cardioembolic stroke
Embolus from the heart gets lodged in intracranial vessels
MCA most commonly affected
Atrial fibrillation is the most common cause
Others: MI, prosthetic valves, rheumatic heart disease
Artery to artery embolism
Thrombus formed on atherosclerotic plaques gets embolized to
intracranial vessels
Carotid bifurcation atherosclerosis is the most common source
Others: aortic arch, vertebral arteries etc.

13. 13
Pathophysiology of Ischemic Stroke
• Blood supply to the brain is autoregulated
• Blood flow
– If zero leads to death of brain tissue within 4-10min
– <16-18ml/100g tissue/min infarction within an hour
• Ischemia leads to development of an ischemic core and an
ischemic penumbra

14. 14
Pathophysiology of Stroke

15. ATP depletion
Hypoperfusion
Failure of Na+
/K+
ATPase membrane ionic pump
Calcium entryGlutamate
release
Activation of lipid peroxidases, proteases & NO
synthase
Destruction of intracellular organelles,
cell membrane & release of free radicals
Free fatty acid release
Activation of pro-
coagulant pathways
Liquefactive
necrosis
Thrombus/embolus
Membrane depolarization & cytotoxic cellular
edema

16. 16
• Tissue surrounding the core region of
infarction which is ischemic but
reversibly dysfunctional
• Maintained by collaterals
• Can be salvaged if reperfused in time
• Primary goal of revascuralization
therapies
Ischmeic Penumbra

17. 17
Hemorrhagic Stroke:
• A small blood vessel in the
brain becomes weak and
ruptures.
• Types of hemorrhagic
stroke:
– Intracerebral hemorrhage
(ICH)
– Subarachnoid hemorrhage

18. 18
Intracerebral Hemorrhage
• Result of chronic hypertension
• Small arteries are damaged due to
hypertension
• In advanced stages vessel wall is
disrupted and leads to leakage
• Other causes: amyloid angiopathy,
anticoagulant therapy, cavernous
hemangioma, cocaine,
amphetamines

19. 19
Subarchanoid Hemorrhage
•Most common cause is rupture
of saccular or Berry aneurysms
•Other causes include
arteriovenous malformations,
angiomas, mycotic aneurysmal
rupture etc.
•Associated with extremely
severe headache

20. 20
Pathophysiology of Hemorrhagic stroke
Explosive entry of blood into the brain
parenchyma which structurally disrupts neurons
White matter fibre tracts are split
Immediate cessation of neuronal function
Expanding hemorrhage can act as a mass
lesion and cause further progression of
neurological deficits
Large hemorrhages can cause transtentorial
coning and rapid death

21. 21
Controllable Risk Factors:
 High Blood Pressure
 Atrial Fibrillation
 High Cholesterol
 Diabetes
 Atherosclerosis
 Circulation Problems
 Tobacco Use and Smoking
 Alcohol Use
 Physical Inactivity
 Obesity
Uncontrollable Risk Factors:
Age
Gender
 Race
 Family History
 PreviousFibromuscular Dysplasia
 Patent Foramen Ovale (PFO or
Hole in the Heart)
 Stroke or TIA
Risk factors

22. 22
The symptoms of a stroke are dependant
on what portion of the brain is damage.
http://www.pdrhealth.com/patient_education/images/BHG01NE13F01.GIF

23. 23
S
Y
M
P
T
O
M
S
• Paralysis or weakness in the face,
arms and/or legs.
• Confusion.
• Personality changes.
• Sudden change in eyesight.
• Decreased motor skills.
• Severe headaches
A sudden development of one or more of the
following symptoms usually indicates a stroke.

24. Clinical Features of Stroke
Anterior ( carotid ) artery
circulation
Posterior ( vertebrobasilar ) artery
circulation
Middle cerebral artery
•Aphasia
•Hemiparesis/plegia
•Hemisensory loss/disturbance
•Homonymous hemianopia
•Parietal lobe dysfunction, e.g.
astereognosis, agraphaesthesia,
impraired two-point discrimination,
sensory and visual inattention, left-right
dissociation and acalculia
Anterior cerebral artery
•Weakness of lower limb more than
upper limb
• Homonymous hemianopia
• Cortical blindness
• Ataxia
• Dizziness or vertigo
• Dysarthria
• Diplopia
• Dysphagia
• Horner’s syndrome
• Hemiparesis or hemisensory loss
contralateral to the cranial nerves
palsy
• Cerebellar signs

25. 25
DIFFERENTIAL DIAGNOSIS

26. 26
SPACE OCCUPYING LESION(TUMOR)
SEIZURE
MIGRAINE
SUBDURAL HAEMATOMA
METABOLIC DISTURBANCE LIKE
HYPOGLYCAEMIA
DIFFERENTIAL DIAGNOSIS

27. 27
DIAGNOSIS

28. 28
DIAGNOSIS

29. 29

30. Figure 6: (a) Carotid Ultrasound
(b) Result(normal)
(c) Result (narrowing)
(a) (b)
(c)

31. 31

32. Figure 7: (a) Leg Ultrasound
(b)Result

33. Stroke management algorithm
Symptoms & signs suggestive of Stroke
Symptoms & signs persist > 1 hour
Acute Care
Urgent Clinical Evaluation
Urgent brain CT
Blood tests
ECG
Ischaemic Stroke
Brain CT normal or shows
acute infarction
Haemorrhagic Stroke
( ICH / SAH )
Brain CT shows haemorhage
Specific Stroke therapy
Thrombolytic therapy ( if
no contraindications ,
Antiplatelet therapy
Neurosurgical
Evaluation & Treatment

34. Acute Stroke Care
Stroke Unit ( if available )
Airway , Breathing , Circulation
Hydration.
Blood Pressure monitoring
Neurological Status monitoring
Anticipate & treat complications
Begin rehabilitation
Neurorehabilitation
Multidisciplinary Team Approach
Proper Positioning
Early mobilization
Physiotherapy
Occupational therapy
Speech therapy
Treat spasticity
Treat depression
Further Investigations
Establish Stroke
subtype and
underlying cause
Cardio &
Cerebrovascular Risk
Assessment
Education
Patient &
Caregiver
Secondary Prevention
Antiplatelet therapy
Treat risk factors
Treat specific underlying cause

35. 35
Treatment
1.Medication

36. 36
2.Surgery

37. 37
Carotid Endarterectomy

38. 38
Prevention

39. 39
Prognosis
• The results of a stroke vary depending on the size and
location, the presence of any associated medical problems,
and the likelihood of recurring strokes.
• Dysfunctions correspond to the area in the brain that had
been damaged.

40. 40
Falij in USM
• The sign and symptoms of Falij which include weakness of
the body rendering the person unable to carry out his daily
activities, strongly simulate with those of stroke
• Falij () is an arabic word derived from the word falj (),
literally means to Halve.
• If Falij affects longitudinal half of the body including face
and neck, is termed as Falij Maa Laqwa or Khala, and the
complete paralysis of the body is said to be Abu Bilqisiya.

41. 41
Etiopathogenesis
The causes of Falij are categorised on two basic underline
pathological processes:
• Sudda or Obstruction in A’asab which hinders the
propagation of Roohe Hassas and Muharrik into the target
organs.
• Roohe Hassas and Muharrik is propagated to the target
organ but due to alterations in Mizaj-e-Tabayi especially
Sue-Mizaj, of the concerned organ,A’asab are unable to
discharge their functions efficiently.

42. 42
• Sudda is resulted in many ways such as any foreign
material pathogenic in nature,Zarba wa Saqta,
displacement of vertebrae, Ghaleez and Luzj Rutubat,
Buhran,Warm, and Imtila
• Fasad in Mizaj It may be due to increased Hararat,
Burudat, Yabusat or Rutubat, but undue Hararat and
Yabusat rarely affects the movements and sensation except
in extreme conditions

43. 43
Pathophysiology
• Elderly people have Barid Mizaj, while children
comparatively have increased Hararat Ghariziya and Rutubat which
encourage body growth and readily replace the wear and tear of
tissues, but as the age advances, Hararate Ghariziya and Rutubat
decreases. It ultimately leads to increased Burudat and Yabusat,
although Hararat is initially reduced with the advancement of age and
causes impairment in Afa'ale Tabiyya, and waste material is not
completely evacuated from the body. The accumulation of morbific
matter results in Hararat-e-Ghareeba with the dominance of Yabusat
occurs, conversely increased Burudat causes altered Haz’m, Taghziya
and Namu. It infers that elderly people are more susceptible to have
Barid Mizaj diseasessuch as Nisyan, Falij, and Ra’sha etc.
• Tabri propounds that initially some parts of the brain are Mumtali
(hyperaemic), suddenly gets dissolved and resultant morbific matter
gets deposited in the weaker portion of the brain. If right ventricle is
weak, there are greater chances of deposition of Barid Balghami
matter and vice versa. If ventricles of both side are weak, morbific
matter gets deposited in both sides resulting in Sakta

44. 44
Falij may be categorised according to aetiology,
character and affected parts paralysed:
On the basis aetiology
Falij Rutubi Balghami:
Falije Damwi:
Falij Intiqali Buhrani
Falij due to Sue Mizaj Sada
 Falije Warami
 Falij due to vertebral
displacement
Falij due to fall, or trauma
On the basis of part affected
Khala/ Falij Maa Laqwa:
Abu Bilqisiya
Sakta
Falije Atrafi
Falije Uzwi
Isterkhai Masana
Isterkhai Lisan
Isterkhai Khanjara:

45. Principles of treatment of Hemiplegia
Falij Nisfi
(Hemiplegia)
Tanqia
(Evacuation of morbidmaterial)
Tanqia
(Evacuation of morbidmaterial)
Tadeel wa Taqwiyat
(Normalization & Revitalization)
Tadeel wa Taqwiyat
(Normalization & Revitalization)
•Har huboob
•Har itrifalat
•Har joshanda
•Har majoon
•Har nutool
•Har zimad
•Har takmeed
•Har saoot
•Har shamoom
•Har inkabab
•Riyazat
(physio)
Munzij balgham
advia
(concoctives)
Dawayein wa Tadabeer
(Drugs & regimens)
Mushil balgham
advia
(purgatives)
Step no. 1 Step no. 2
Make Balgham (phlegm)
evacuable
Purgate out Balgham
(phlegm)

46. Management of Falij Nisfi (Hemiplegia)
Falije Nisfi is usually a Balghami disease, hence, the treatment is
formulated on the line of ‘Tanqiya wa Tadeel’
Phase of Tanqiya (Evacuation):
1st
day -Maul Asl (Honey water) = honey
25 ml and water 100 ml boil to
half and serve for 5-7 days
Nuskha Munzij Balgham (concoctives)
Properties: Taqtee, Tahleel wa Talteef
Vs
Thrombolysis, Antithrombosis, Neuroprotection
• Badyan 7 gms, Bekh badyan-- 5 gms
• Bekh karafs 5 gms Bekh izkhar--5 gms
• Bekh kasni 5 gms ,Unnab 10 no.
• Mako khushk 5 gms, Ustukhuddus 5gms
• Badranjboya 5 gms, Parsiyaoshan 5 gms
• Gauzaban 5 gms ,Aslassoos 5 gms
• Khatmi 5 gms, Gul Banafsha 5 gms
Prepare Joshanda (decoction) and serve with
Khamira Banafsha 25 gms in the morning
for 12 days.

47. On 18th
day:
Mushil balgham (purgatives- for whole body):
• Turbud ------------------------------- 7 gms
• Berg sana --------------------------- 9 gms
• Turanjbeen -------------------------- 25 gms
• Sheere khisht ------------------------ 25 gms
• Maghz faloos khayar shambar --- 25 gms
• Roghan badam ---------------------- 5 gms
The contents of Mushil Balgham are added with
Munzij Balgham, boiled and served
On 19th
day:
Nuskha Tabreed (cooling drugs):
• Tukhme asapghol ------------------- 4 gms
• Tukhme kanocha -------------------- 4 gms
• Tukhme bartang --------------------- 4 gms
• Tukhme reehan ---------------------- 4 gms
Luab is obtained, mixed with Sharbat Banafsha
20 ml. and served
On 20th
and 21st
days:
Only Munzij Balgham (concoctives) is
continued.
On 22nd
day:(For Tanqiya khaas--brain)
Hab Ayaraj 6 no. at 5 a. m. with Arq Gauzaban
125 ml. Followed by—
Nuskha Munzij Balgham and Mushil Balgham
(without Maghz faloos khayar shambar and
Roghan badam) at 6:30 a. m.

48. On 23rd
day:
• Munzij and mushil are stopped .
Tanqiya (evacuation) is completed
Phase of Tadeel wa Taqwiyat
(Normalization and potentiation):
• Gharghara (gargles)
• Shamoom (aromatherapy)
• Haar majoon (semi- solid polyherbal prep.)
• Haar Roghaniyat for Dalk (Massage)
• Saoot (Nasal drops)
• Atoos (Sternutative)
• Nafookh (Nasal insufflation)
• Nushooq (snuff)
• Mazoogh (Chewing drugs)
• Inkabab (Steam bath)
• Nutool (Irrigation)
• Zimad (Ointments)
• Takmeed (Poulticing)
• Tila (Liniment)
• Riyazat (Exercise)

49. CONCLUSION
• Stroke - sudden death of brain cells due to lack of oxygen
• Caused by blockage of blood flow / rupture of artery to the
brain
• Symptoms: weakness / paralysis on one side of the body
difficulty with balance, speaking, swallowing
• Clot-busting drugs like TPA can be used to reverse a stroke
• Prevention - minimizing risk factors
(controlling high blood pressure, high cholesterol, diabetes)

50. 50