and primarily occurs in the posterior portion of the cerebral hemispheres. Brain tissue perfusion is inadequate due to abnormal channels between the arterial and venous systems that allow mixing of oxygenated and unoxygenated blood, resulting in increased venous pressure, which causes engorgement and dilation of the venous structures. AVMs range in size from a few millimeters to large malformations that extend from the cerebral cortex to the ventricles. In fact, if the AVM is large enough, the shunting can deprive the surrounding tissue of adequate blood flow, resulting in cardiac decompensation— where the heart can’t pump enough blood to compensate for bleeding in the brain (typical in infants and small children). Thin-walled vessels may ooze small amounts of blood—they may even rupture—causing hemorrhage into the brain or subarachnoid space.
Development of cerebral aneurysm and subsequent rupture
Hemorrhage (intracerebral, subarachnoid, or subdural, depending on the location of the AVM)
Hydrocephalus
chronic mild headache, a sudden and severe headache, or a localized or general headache
seizure
vision disturbances
muscle weakness or inability to move a limb or a side of the body
lack of sensation in part of the body, or abnormal sensations, such as ringing and numbness
mental status change (sleepy, stuporous, lethargic, confused, disoriented, or irritable)
stiff neck
impaired speech or sense of smell
fainting, dizziness, and decreased level of consciousness
facial paralysis, eyelid drooping, and tinnitus.
Magnetic resonance imaging identifies irregular or globoid masses; however, hemorrhage may obscure findings.
Cerebral arteriogram confirms the presence of AVMs and evaluates blood flow.
Doppler ultrasonography reveals abnormal, turbulent blood flow.
Computed tomography scan identifies intracerebral hemorrhage and large AVMs.
surgery carries a higher risk because the surgery itself may cause the AVM to bleed uncontrollably.
about arteriovenous malformation (AVM) and its implications
about prescribed medication administration, dosage, possible adverse effects, and when to notify the physician
postoperative care of any incision
activity recommendations
signs and symptoms of complications, such as shunt infection or intracranial bleeding (sudden severe headache, vision changes, decreased movement in extremities, and change in level of consciousness)
the importance of follow-up care
the benefits of utilizing available community resources or support groups, especially if neurologic deficits have occurred.
Monitor vital signs and titrate medications to control hypertension.
Monitor neurologic status.
Monitor for seizure activity and institute seizure precautions.
Maintain a quiet atmosphere and provide relaxation techniques.
Provide appropriate education to the parents (and patient if appropriate) before discharge. (See Teaching the patient with an AVM, page 189.)
impaired motor function and cognition. Even though defects are present at birth, signs and symptoms may not be apparent until months later, when the axons have become myelinated and the basal ganglia are mature.
Prenatal conditions that may increase risk of CP: maternal infection (especially rubella), maternal drug ingestion, radiation, anoxia, toxemia, maternal diabetes, abnormal placental attachment, malnutrition, and isoimmunization.
Perinatal and birth difficulties that may increase the risk of CP: forceps delivery, breech presentation, placenta previa, abruptio placentae, metabolic or electrolyte disturbances, abnormal maternal vital signs from general or spinal anesthetic, prolapsed cord with delay in delivery of head, premature birth, prolonged or unusually rapid labor, and multiple birth (especially infants born last in a multiple birth).
Infection or trauma during infancy that may increase the risk of CP: poisoning, severe kernicterus resulting from erythroblastosis fetalis, brain infection, head trauma, prolonged anoxia, brain tumor, cerebral circulatory anomalies causing blood vessel rupture, and systemic disease resulting in cerebral thrombosis or embolus.
Contracture
Skin breakdown and ulcer formation
Muscle atrophy
Malnutrition
Seizure disorders (in about 25% of patients)
Speech, vision, and hearing problems
Language and perceptual deficits
Mental retardation (in up to 40% of patients)
Dental problems
Aspiration pneumonia
excessive lethargy or irritability
high-pitched cry
poor head control
weak sucking reflex
smaller than normal head circumference
abnormal postures
abnormal reflexes
abnormal muscle tone. (See Assessing signs of cerebral palsy.)
underdevelopment of affected limbs
characteristic scissors gait
hyperactive deep tendon reflexes and increased stretch reflexes
rapid alternating muscle contraction and relaxation
muscle weakness
muscle contraction in response to manipulation with a tendency toward contractures.
involuntary movements, such as grimacing, wormlike writhing, dystonia, and sharp jerks that impair voluntary movement
involuntary facial movements (affects speech).
lack of leg movement during infancy
wide gait
disturbed balance
incoordination (especially of the arms)
hypoactive reflexes
nystagmus
muscle weakness and tremors
lack of sudden or fine movements.
TYPE OF CP | SIGNS AND SYMPTOMS |
---|---|
Spastic CP (due to impairment of the pyramidal tract [most common type]) |
|
Athetoid CP (due to impairment of the extrapyramidal tract) |
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Ataxic CP (due to impairment of the extrapyramidal tract) |
|
Mixed CP |
|
retarded growth and development
difficulty chewing and swallowing.
Cranial ultrasound identifies structural abnormalities, hemorrhage and hypoxic-ischemic injury.
Computed tomography scan and magnetic resonance imaging may show congenital malformations, hemorrhage, and periventricular leukomalacia.
EEG may identify the source of seizure activity.