Treatment of spasticity

Pharmacologic therapies Nonpharmacologic

therapies

Injections
Oral Physiotherapy
drug Surgical
Intrathecal
therapies drug
therapy
 Botulinum toxin (Botox)

§ Botox is injected into target muscles and works to reduce

muscle activity by blocking acetylcholine release at the
neuromuscular junction.
§ Spasticity is reduced because of the localized reduction in
muscle activity without affecting the CNS control
parameters of movement.
§ The timing of the effects varies with dosage (Generally
the effect peaks about 3 to 4 weeks after injection and
may last for several months).
§ This reduction in muscle activation provides a window of
opportunity for an intense period of physical therapy to
improve motor control factors ,
 Baclofen
§ Baclofen, a gamma-amino butyric acid agonist.
§ It acts at the spinal cord level to impede the release of
excitatory neurotransmitters believed to mediate spasticity.
§ Continuous intrathecal Baclofen infusion has been used to
treat spasticity in children with CP & adults with CVA,
traumatic brain injury (TBI), and multiple sclerosis (MS).
§ When administered intrathecally, Baclofen can be given in
adequate dosage to reduce spasticity without the stuporous
side effects associated with oral administration.
§ Baclofen appears to be effective in reducing spasticity and
improving function in selected cases.
§ It appears most effective in individuals with severe
spasticity.
 ACA

MCA

MCA ACA
PCA PCA
Cerebral Arteries
(anterior view)
Complete oclusion of the artery is maniefested by:

ž Ipsilateral blindeness
ž Contralateral Hemiplegia
ž Contralateral hemihyposthesia
ž Contralateral homonymous hemianopia.
ž Aphasia with or without agraphia in Lt. sided lesion
- It supplys the lateral aspect of anterior (⅗) of the cerebral
hemisphere
- Most Commonly affected vessel.
§ Coma at onset
§ Contralateral Hemiplegia (affecting UL
> LL
§ Contralateral hemihyposthesia with
cortical sensory loss in UL.
§ Contralateral homonymous hemianopia.
§ Aphasia & agraphia in Lt. sided lesion

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- It supplys the medial aspect of anterior (⅗) of the cerebral
hemisphere & upper edge of the lateral surface
ž Contralateral Hemiplegia (affecting LL > UL

ž Contralateral cortical sensory loss in LL.

ž Contralateral homonymous hemianopia.
ž Mentality & Personality changes
ž Urine incontinence.
ž Forced grasp reflex
- It supplys the posterior (⅖) of the cerebral hemisphere
(occibital lobe + post. Part of temporal lobe)

ž Contralateral homonymous hemianopia.

ž Visual agnosia in Lt. sided lesions.
ž Thalamic syndrome: in case of interruption of bl.
Supply to thalamus (thalamo-geniculate artery)

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ž Complete contralateral Hemianasthesia to all types of
sensations with partial recovery of superficial sensation,
however vibration sense is permenantly lost.
ž Thalamicpain: i.e., constant burning severe pain in the
hemianaethetic side.
ž Involuntarymovements (e.g., choreo-athetosis) due to
ischemia of basal gangalia.
 Transient Ischaemic Attacks
(TIAs)

Neurological Diseases and its Surgery TIAs 2nd Semester 1445 H

Definition:
A transient attack of neurological dysfunction caused by
focal transient brain ischemia, with clinical symptoms
typically lasting minutes up to one hour without evidence of
infarction on brain imaging.

q Most TIAs last about 2-20 minutes.

q If a patient still has symptoms > an hour after the onset, the
chances are that they will persist > 24 hour & so the patient
will actually have had a stroke.
If ischemia lasts over 24 hours and then the patient recovers, it is
termed Reversible Ischaemic Neurological Deficit
(RIND).

TIAs and RIND are important warning signs for

the development of cerebral infarction.
 Causes of TIAs

- Microemboli - Vasculitis
a) From artery to artery: arising - Vaso-spasm
from atheromatous plaques in large - Hyperviscosity: (e.g.,
bl vessels (e.g., Carotid to MCA) polycythaemia)
b) Cardiogenic (heart to artery). - These are less common
- This is the most common cause. Causes.

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ž A temporary reduction or stoppage of cerebral bl. flow in a
specific neurovascular distribution as a result of partial or
total occlusion.
ž Clinical manifestations vary depending on the vessel
involved & the cerebral territory it supplies.
ž TIAs can involve any cerebral artery
ž They may precede the development of stroke, or can occur
by themselves without leading to stroke.
ž ~ 20% of infarcts that follow the TIAs occurs within a
month after the first attack & ~ 50% within a year.
 (The symptoms are typically sudden & abrupt)

ž Motor symptoms (the most common):

Weakness or heaviness in UL, LL or face on one side of
the body
ž Sensory symptoms: Numbness/tingling
ž Transient Monocular Blindness (Amaurosis Fugax):
Momentary visual loss from transient retinal ischemia.
Suspect an ICA source of emboli. Affect the upper or
lower half of vision, or all the vision of one eye & often
described like a blind or shutter coming down from above,
or up from below 22
 Clinical Picture of TIAs
The patients present with the manifestations of either:

Carotid insufficiency Vertebro-basilar insufficiency

Carotid system supplies ant. 3/5 of brain) Vertebro-basilar system supplies Post. 2/5 of brain)

One or more of the following: One or more of the following:

- Hemiparesis -Hemiparesis/Hemianasthesia
- Hemihyposthesia (sensory fibers in Internal capsule) - Syncope
- Aphasia/agraphia (in dominant hemisphere) - Ataxia
- Convulsions (due to temporal lobe affection) - Diplopia
- Unilateral blindness (due to optic N. affection) - Ophthalmoplegia
- Mentality changes (frontal lobe affection) - Vertigo /Unsteadiness
- Circumoral numbness
- Bulbar symptoms 23
1- Doppler ultrasonic imaging:
It is used on the neck vessels and it maps out an image of
the moving column of blood in the vessel (dynamics of the
blood).

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2- Real time (B mode) ultrasound imaging:
It shows a longitudinal or transverse section of the vessel.
It measures the thickness of the carotid arteries.

3- Digital subtraction angiography:

It visualizes the intracerebral vessels.
It is non-invasive as it requires a contrast medium given I.V.

4- Cerebral angiography:
It is invasive and requires a contrast medium injected directly
into the artery via a catheter. Imaging by X-ray.
It is the most precise method, showing any occlusion or
stenosis in the cerebral vascular tree. 25
Cerebral angiography

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5- Magnetic Resonance Angiography (MRA):

It is a type of magnetic resonance imaging that uses harmless

but powerful magnetic fields to give a detailed picture of the
arteries in the brain.

6- Investigations for the risk factors:

As blood glucose, serum uric acid, cholesterol level,
hypertension.

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 Treatment of patients with TIAs
A. Medical treatment:
1) Antiplatelet aggregating drugs.
2) Anticoagulant drugs.

3) Drugs to increase blood supply to the brain.

4) Treatment of any risk factors.

B. Surgical treatment:
1) Endarterectomy.
2) Carotid angioplasty
They are used in carotid artery stenosis > 70%. Not used in mild
stenosis or if a stroke already occured
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 Carotid endarterectomy
(CEA)
- It is a surgical procedure used to reduce
the risk of stroke, by correcting stenosis
(narrowing) in the common carotid
artery or internal carotid artery.

- Endarterectomy is the removal of the

accumulated material on the inside
(endothelium) of an artery.

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 Carotid Angioplasty (Carotid stenting)

- Procedure that opens clogged arteries to

prevent or treat stroke.
- It is often combined with placement of a
stent (small metal coil) in the clogged artery.
- The stent helps prop the artery open and
decreases the chance of its narrowing again.
- Carotid angioplasty and stenting may be used
when traditional carotid surgery isn't feasible
or is too risky

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