A Flashcards

1
Q

What are the branches of the vertebral artery?

A

1-To the meninges
2- Anterior and posterior spinal arteries to the spinal cord.
3- Posterior inferior cerebellar artery to the cerebellum.
4- Small penetrating arteries to the medulla.

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2
Q

What are the branches of the basilar artery?

A

● The anterior inferior cerebellar artery.
● The superior cerebellar artery.
● The internal auditory artery.
● Small penetrating branches to the brain stem.

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3
Q

How is the cerebral blood flow regulated?

A

1- Arterial CO2 tension → arise of Pa CO2 of 1mm Hg →causes an immediate increase in CBF of 5%.
2- Arterial O2 tension → its effect is less than that of CO2.
3- Blood viscosity (hematocrit) → CBF is inversely related to the whole blood viscosity.
4- Arterial blood pressure: CBF remains constant when the mean systemic blood pressure is between 60-160mmhg which is known as auto regulation.
- Decrease systemic arterial blood pressure → vasodilatation → increase CBF → until exhaustion occurs → oligemia and ischemia.
- Increase systemic blood pressure → vasoconstriction →decrease CBF → until exhaustion occurs→ hyperemia and ischemia.
- In chronic hypertensive patients, the auto regulation range is shifted upwards.
- Auto regulation is impaired in:
- Previously damaged brain (e.g., old stroke, trauma …)
- Elderly.
- Organ failure.
- Metabolic impairment.

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4
Q

Risk factors of stroke?

A

1) Age
2) Sex
3) Hypertension
4) DM
5) Cardiac diseases
6) Dyslipidemia
7) Hyper-coagulability
8) Alcohol consumption
9) Coffee
10) Cigarette smoking
11) Dietary habits
12) Drug induced stroke:
- Hypotensive drugs.
- Cytotoxic drugs → thromboembolic strokes.
-Aspirin, anticoagulants, thrombolytic therapy.
13) Contraceptive pills
14) History of TIA or stroke.
15) Family history of stroke.
16) Lower social class.
17) Body built
18) Physical inactivity.
19) Chronic stress.

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5
Q

Causes of hemiplegia

A

1- Vascular (STROKE): either ischemic or hemorrhage.
2- CNS infections: brain abscess, encephalitis.
3- Brain tumors: meningioma, glioma, etc..
4- Demyelinating: DS, DEM.
5- Trauma: cerebral laceration, subdural hematoma.
6- Congenital cerebral palsy.
7- Hysterical: the patient suffers from paralysis although there is no organic
pyramidal tract lesion.

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6
Q

Mid brain syndromes (Hemiplegia)

A

1)Weber’s syndrome:
- Ipsilateral 3rd cranial nerve lesion
- Crossed hemiplegia (contra lateral).
2) Benedict’s syndrome: as above+ hemiataxia on the opposite site of the lesion (red nucleus affection).

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7
Q

Pons syndromes (Hemiplegia)

A

1) Millard Gubler’s syndrome:
- Ipsilateral 6th, 7th cranial nerves lesion
- Crossed hemiplegia.
2) Foville’s syndrome:
- Crossed hemiplegia.
- Ipsilateral loss of conjugate eye movement.

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8
Q

Medullary syndromes (Hemiplegia)

A

1) Wallenberg syndrome:
- Ipsilateral
- Horner’s syndrome
- Ataxia
- 9, 10, 11th cranial nerves
- Decrease sensation over the face
- Contra lateral hemianathesia.
2) Avillis syndrome:
- crossed hemiplegia.
- ipsilateral 9th &10th Cr. N paralysis.
3) Jackson’s syndrome: crossed hemiplegia+ ipsilateral 11th&12 Cr. N.

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9
Q

Risk factors of ischemic stroke

A
  • Old Age (>65 y) [75% of all strokes].
  • Race (African>Hispanics >Caucasians.
  • Sex (Male more).
  • Family history of ischemic stroke.
  • Previous stroke, Transient ischemic attacks, or myocardial infarction.
  • AF, Hypertension, Diabetes mellitus, Dyslipidemia, Smoking, Obesity, and physical inactivity.
  • Cardiovascular disease and coronary artery disease.
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10
Q

Pathophysiology of ischemic stroke?

A

▪ Ischemic stroke is caused by focal cerebral ischemia: a localized reduction in blood flow sufficient to disrupt neuronal metabolism and function.
▪ If ischemia is not reversed within a critical period, irreversible cellular injury ensues, resulting in cerebral infarction.
▪An area called a PENUMBRA may result, denotes the part of an acute ischemic stroke that is at risk of progressing to infarction but is still salvageable if reperfused. It is usually located around an infarct core (which represents the tissue which has already infarcted or is going to infarct regardless of reperfusion).
▪ The primary aim of current acute stroke intervention is to prevent the penumbra from proceeding to established infarct.

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11
Q

Inclusion criteria of Thrombolysis with recombinant tissue plasminogen activator

A
  1. Symptoms suggestive of ischemic stroke that believed to be disabling.
  2. Able to initiate treatment within 4.5 h of Time Last Known Well.
  3. Age 18 y or older.
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12
Q

Contraindications of Thrombolysis with recombinant tissue plasminogen activator

A
  1. Intracranial hemorrhage (e.g., ICH or SAH) history or presence on imaging.
  2. Brain CT demonstrates large infarction.
  3. Elevated Blood pressure greater than 185/110 mm Hg.
  4. Recent (within 3 months) severe head trauma or neurosurgical operation.
  5. INR >1.7, thrombocytopenia, recent use of heparin or direct oral anticoagulants).
  6. Intracranial neoplasm, or aneurysm.
  7. Active internal bleeding.
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13
Q

Complications of Thrombolysis with recombinant tissue plasminogen activator

A

1) Bleeding.
2) Intracranial and extracranial hemorrhage.
3) Angioedema

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14
Q

Pathophysiology of hemorrhagic stroke?

A

1) Blood from an ICH accumulates as a mass that can dissect through and compress adjacent brain tissues, causing neuronal dysfunction.
2) Large hematomas increase ICP.
3) If the hemorrhage ruptures into the ventricular system (IVH), blood may cause acute hydrocephalus.
4) Cerebellar hematomas can expand to block the 4th ventricle, also causing acute hydrocephalus.
5) Midbrain or pontine hemorrhage, IVH, or acute hydrocephalus can impair consciousness leading to coma and death.

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15
Q

Risk factors of Subarachnoid hemorrhage?

A

Controllable
● Smoking.
● Alcohol
● Certain drugs abuse.
● Poorly controlled hypertension.

Uncontrollable
* Family & personal history of SAH.
* Female sex.
* Aneurysm.

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16
Q

Causes of Subarachnoid hemorrhage?

A

1) Rupture of an intracranial aneurysm (commonest cause) which might be:
a) Congenital b) Atherosclerotic c) Mycotic
2) Rupture of an intracranial arterio-venous malformation (AVM).
3) Blood diseases: purpura, leukemia.
4) Severe hypertension as in eclampsia.
5) Head trauma.
6) Hemorrhage in a brain tumor.
7) Wrong administration of anticoagulants.

17
Q

Pathophysiology of Subarachnoid hemorrhage?

A
  • The rupture of an aneurysm results in the release of blood into the subarachnoid space temporarily. Continuous bleeding is ultimately not possible in a confined space, as such results in rapid death.
  • Should bleeding be brief, potentially stemmed by the sudden rise in ICP, the patient may survive to present for medical attention. Re-rupture is possible and often fatal.
18
Q

Clinical Picture of Subarachnoid hemorrhage?

A

1- Sudden severe headache.
2- Depressed consciousness.
3- Stiff neck / meningism.

19
Q

complications of Subarachnoid hemorrhage?

A

1) Rebleeding: its prognosis is worse than the initial bleeding.
2) Cerebral vasospasm (Focal cerebral ischemia because of cerebral artery vasospasm is the greatest cause of neurological morbidity). Usually occurring
between 4-14 days post-ictus.
3) Hydrocephalus: 10-20% due to either intraventricular extension of the hemorrhage or obstruction of CSF drainage by blood.
4) Epilepsy: due to cortical irritation and damage.

20
Q

Compare the 3 types of focal (Partial) Seizures.

A

a- Simple partial seizures (SPS): b- Complex partial seizures (CPS):
⬥ No aura VS⬥ Preceded by aura in 1/3rd of cases (fear, photophobia…).
⬥ No automatism. VS ⬥ Automatism may occur
⬥ No loss of consciousness. VS ⬥ Consciousness is impaired.
⬥ May be motor, sensory or autonomic fits. VS⬥ Only motor fits occur.

c- Partial seizures with 2ry generalization:
⬥ Focal seizures followed by generalization (involvement of whole body).

21
Q

What are absence seizures (Petit mal)?

A

⬥ Sudden cessation of all motor activities and speech (Awareness of the surroundings is cut off).
⬥ Precipitated by hyperventilation or photic stimulation.
⬥ Rarely persists more than 30 seconds (but frequently recurrent).
⬥ Usually not associated with loss of consciousness.
⬥ No aura.
⬥ No post-ictal phase.

22
Q

What are generalized tonic-clonic seizures (Grand mal)?

A

❖ The commonest type, passes into 3 phases:
1- Aura (pre ictal): Before the attack as a warning sign which may be motor (localized muscular spasms), sensory (paresthesia) or autonomic (intestinal
pain).
2- Attack (Ictal):
-Sudden loss of consciousness (not more than 10 min).
-Tonic phase: Rigid posture with rolling of the eyes, drooling of saliva, clinching of the teeth and incontinence to urine and stool.
- Clonic phase: Rapid relaxation and contraction of muscles (clonic motor activity).
3- Post ictal phase: Headache, sleep or Todd’s paralysis.

23
Q
A