cerebral

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cerebral

 [ser´ĕ-bral, sĕ-re´bral]
pertaining to the cerebrum.
cerebral palsy a diagnostic term used to describe a type of nonprogressive neuromotor dysfunction; it is a disorder of movement and posture resulting from an insult to the immature brain. Cerebral dysfunction can occur because the central nervous system has not developed properly from the start (a developmental anomaly); or it can be the consequence of an injury to a previously normally developing nervous system. The insult of cerebral palsy is always static and nonprogressive; the lesion itself will not get worse. What often do change over time are the manifestations of the motor disorder and the emergence or recognition of associated deficits as the child grows and the nervous system matures. There is no universally accepted age-of-onset criterion for making the diagnosis. The upper age limit is often set at seven or eight years old for an acquired insult to be classified as cerebral palsy; this is the age when motor areas in the nervous system have largely reached maturation and therefore the potential for motor plasticity significantly diminishes. Prior to this age, function lost by damage to one area of the brain may be partially taken over by another area. However, there is not universal agreement on this age criterion.

The child with cerebral palsy is at high risk for having associated deficits in neurological, cognitive, and perceptual abilities. Motor deficits are generally identified before delays in language or perceptual abilities are evident.
Etiology. Cerebral palsy is relatively common, affecting 1 in 200 children. This number takes into account the full spectrum of the disorder, including milder cases, a broad definition of age of insult, and more complete case ascertainment. The exact cause cannot always be determined, but it usually develops before the age of three. The percentage due to prenatal anomalies and insults is usually considered to be 40 to 60 per cent. Damage to the fetal brain can occur as a result of maternal infections, drug or alcohol abuse, other teratogenic exposures, and genetic syndromes. Cerebral palsy is associated with preterm birth between 30 and 50 per cent of the time, but it is not clear whether or not this association is causal in nature. Thirty years ago, the belief was that most cerebral palsy was a consequence of birth-related injury to the brain, and obstetricians often took blame for “causing” the condition. More recently, there has been a shift in emphasis to unknown prenatal events as the causative factors, such as preterm birth, difficult deliveries, and prenatal or perinatal brain injuries. Any situation that interferes with the fetal oxygen supply can produce brain damage and cerebral palsy. These include premature separation of the placenta, prolapsed cord, and chronic placental insufficiency. Other potential causes during the perinatal and early postnatal period include hypoglycemia, which can lead to cell death; hypernatremia, which results in cellular hyperosmolality, vascular lesions, and intracranial hemorrhage; and hyperbilirubinemia. Postnatally acquired cerebral palsy is usually considered to be around 10 per cent of cases. Damage to the brain in childhood can result from infections of the meninges or brain cells; near-drowning or similar anoxic insults; cancers that although successfully treated leave permanent brain damage; head injury; or any of various stroke syndromes.
Classification. The most common classification for cerebral palsy, based on the predominant clinical manifestations, distinguishes three major types: (1) spastic, in which there are exaggerated stretch reflexes, muscle spasticity, and a strong tendency to develop contractures; (2) athetoid, with purposeless, uncontrollable movements and muscle tension; and (3) atactic, in which the child has poor balance, poor coordination, and a staggering gait.
Treatment. This varies according to the nature and extent of brain damage. Muscle relaxants and other medications may help reduce spasms. Orthopedic surgery, casts, braces, and traction can be used to correct or prevent associated deformities. Early muscle training and special exercises may also promote function, prevent deformity, and help the child lead a useful, productive life. If muscle training is not begun early, extensive rehabilitation may be necessary to correct faulty habits and poor muscle patterns the child has established. However, it is never too late for a complete evaluation of the condition of a patient with cerebral palsy. A rehabilitation program can produce good results later in life, not only in childhood. Anticonvulsant drugs are necessary when seizures are among the associated symptoms. Special education is important for children with cognitive impairments, as is attention to the other associated problems.

ce·re·bral

(ser'ĕ-brăl, se-rē'brăl), Although the pronunciation of this word with stress on the first syllable is classically correct, the second syllable is often stressed in the U.S.
Relating to the cerebrum.

cerebral

(sĕr′ə-brəl, sə-rē′-)
adj.
1. Of or relating to the brain or cerebrum.
2. Appealing to or requiring the use of the intellect; intellectual rather than emotional: "His approach is cerebral, analytical, cautious" (Helen Dewar).

cer·e′bral·ly adv.

hypertension

High blood pressure Cardiovascular disease An abnormal ↑ systemic arterial pressure, corresponding to a systolic BP of > 160 mm Hg and/or diastolic BP of 95 mm Hg and graded according to intensity of ↑ diastolic BP; HTN affects ± 60 million in the US Workup Evaluation of HTN requires clinical Hx for Pt, family Hx, 2 BP determinations, funduscopy, ID of bruits in neck & abdominal aorta, evaluation of peripheral edema, peripheral pulses and residual neurologic defects in stroke victims, chest films to determine cardiac size and lab parameters to rule out causes of secondary HTN Risk factors Race–blacks more common, ♂, family history of HTN, obesity, defects of lipid metabolism, DM, sedentary lifestyle, cigarette smoking, electrolyte imbalance–eg, ↑ sodium, phosphorus, ↓ potassium, tin Treatment Diet–eg, sodium restriction, ↓ calories, alcohol and cigarettes–the weight gain accompanying smoking cessation tends to offset the minimal ↓ in BP, calcium supplements, lifestyle manipulation–eg, biofeedback, ↑ exercise; antihypertensives–eg, diuretics–benzothiadiazines, loop diuretics, potassium-sparing diuretics, sympatholytic agents–central and peripheral-acting α-adrenergics, β-adrenergics, mixed α- and β-blockers, direct vasodilators, ACE inhibitors–the preferred agent to use ab initio, dihydropiridine CCBs. See ACCT, ACE inhibitor, Borderline hypertension, Borderline isolated systolic hypertension, Calcium channel blocker, Drug-induced hypertension, Essential hypertension, Exercise hypertension, Familial dyslipemic hypertension, Gestational hypertension, Idiopathic intracranial hypertension, Isolated systolic hypertension, Malignant hypertension, MRC, Obetension, Paradoxic hypertension, Pill hypertension, Pregnancy-induced hypertension, Pseudohypertension, Pulmonary hypertension, Refractory hypertension, Renovascular hypertension, SHEP, STOP-Hypertension, TAIM, TOHP-1, TOMHSTyramine hypertension, White coat hypertension.
Hypertension
Class I–mild Diastolic pressure 90-104 mm Hg
Class II–moderate Diastolic pressure 105-119 mm Hg
Class III–severe Diastolic pressure > than 120 mm Hg
Hypertension types
Essential hypertension Idiopathic HTN The major form comprising 90% of all HTN
Malignant hypertension A sustained BP > 200/140 mm Hg, resulting in arteriolar necrosis, most marked in the brain, eg. cerebral hemorrhage, infarcts, and hypertensive encephalopathy, eyes, eg papilledema and hypertensive retinopathy and kidneys, eg acute renal failure and hypertensive nephropathy; if malignant HTN is uncorrected or therapy refractory, Pts may suffer a hypertensive crisis in which prolonged high BP causes left ventricular hypertrophy and CHF
Paroxysmal hypertension Transient or episodic waves of ↑ BP of any etiology, punctuated by periods of normotension, typical of pheochromocytoma
Portal hypertension ↑ portal vein pressure caused by a backflow of blood through splenic arteries, resulting in splenomegaly and collateral circulation, resulting in esophageal varices and/or hemorrhoids; PH may be intra- or extrahepatic, and is often due to cirrhosis, or rarely portal vein disease, venous thrombosis, tumors or abscesses
Pulmonary hypertension A condition defined as a 'wedge' systolic/diastolic pressure > 30/20 mm Hg–Normal: 18-25/12-16 mm Hg, often secondary to blood stasis in peripheral circulation, divided into passive, hyperkinetic, vasoocclusive, vasoconstrictive and secondary forms. See Pulmonary HTN.
Renovascular hypertension see there.
Secondary hypertension
Aging
Cardiovascular Open heart surgery, coarctation of aorta, ↑ cardiac output–anemia, thyrotoxicosis, aortic valve insufficiency
Cerebral ↑ Intracranial pressure
Endocrine Mineralocorticoid excess, congenital adrenal hyperplasia, glucocorticoid excess, eg Cushing syndrome, hyperparathyroidism, acromegaly
Gynecologic Pregnancy, oral contraceptives
Neoplasia Renin-secreting tumors, pheochromocytoma
• ↓ Peripheral vascular resistance AV shunts, Paget's disease of bone, beri-beri
Renal disease Vascular, parenchymal

ce·re·bral

(ser'ĕ-brăl)
Relating to the cerebrum.

cerebral

1. Pertaining to the cerebrum or brain.
2. Having the quality of intellectualism.

Cerebral

Pertaining to the brain.
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