Transient ischemic attack (TIA)
The most common cause of TIA are cerebral embolus originated by atherosclerotic plaques in the carotid or vertebral arteries, or the sharp reduction of blood flow through the arteries with stenosis.
TIAs appear suddenly, last between 2 and 30 minutes or more, and then subside without leaving neurological sequels, with an intact consciousness level during the episode.
When carotid artery is affected, the symptoms are usually unilateral, with homolateral blindness, contralateral hemiparesis, and frequent paresthesia and dysarthria. The aphasia indicates the involvement of the dominant hemisphere.
When the vertebrobasilar system is affected, there can be confusion, dizziness, binocular blindness, or diplopia, and weakness with paresthesia of the extremities, with possibility of falling on the floor. Dysarthria can appear.
The patients with transient brain ischemia have a probability of 43% of suffering another vascular attack in the next 10 years.
The risk of a vascular event is higher shortly after the ischemic attack, reaching its lower point at 3 years and gradually increasing after this time.
Long-term improvements should be performed in the secondary prevention of the vascular disease in patients with transient brain ischemia.
It has been shown that the improvements in the treatment and control of the risk factors such as HT, diabetes, obesity, hyperlipidemia, and smoking reduce the incidence of cerebral infarction by 40%.
Hypertension is the first risk factor for triggering a stroke, so that our patients should follow a balanced diet, low on salt and comply without interruptions the prescribed treatment.
Antiaggregation and anticoagulant agents are frequently indicated, where there is a risk of embolisms.
Surgical or instrumental approach of carotid atherosclerosis has selected its indication.
The increased number of elderly population would suggest an increase in the incidence of diseases related with aging, including cerebral infarction.
However, the improvements in medical prevention with the use of blood pressure and cholesterol lowering drugs, reduction of adverse reactions related to these drugs, and the surgical prevention of infarction have reduced the risk of cerebral ischemia in those over 60 years of age.
Advice on transient ischemic attack (TIA)
It is difficult to advise against driving in a patient who at the time of the consultation is feeling well, but suffers recurrent TIA with the risk of losing the control of the car.
If the preventive treatment is not possible or effective, and the TIAs occur, the patient cannot drive.
It is not advised to drive until at least 6 months after the TIA, without neurological symptoms, with a medical report from the neurologist specifying that there are no sequels, and with short effective terms of the driving license.
The problem arises when the population ages and the first episode occurs while driving.
Patients on anticoagulants should be warned of their greatest risk to suffer bleeding with minor blows, so that they maximize the caution when driving.
The patients who despite medical therapy suffer TIA cannot drive either.
Stroke in progress and established
Stroke in progress is defined as the infarction of growing size that occurs for neurological disorders, that increase within a period of 24-48 hours.
Acute established stroke is the most common disorder, where the symptoms appear fast and reach a peak in a few minutes.
Neurological disorders can worsen on the next days with possible reduction of the level of conscience. The subsequent improvement is gradual for days, weeks or months, except in serious infarctions.
It most commonly affects the territory of the medial cerebral artery, leading to contralateral hemiplegia with hemianesthesia and homonymous hemianopsia. Aphasia occurs if the dominant hemisphere is involved and apraxia if it is the non-dominant.
Complete occlusion of the basilar artery usually causes ophthalmoplegia, pupillary disorders, tetraparesis or tetraplegia, and disorders in the level of conscience. Often, dysarthria, dysphagia and emotional instability. The outcome is poor.
The degree of final neurological recovery depends on the age of the patient, his general health condition and the localization and size of the infarction. Complete recovery is uncommon, but the earlier the improvement starts, the better the prognosis.
The impairment in the level of consciousness and mental, aphasia, and serious signs of the encephalic trunk involve a poor prognosis.
Approximately half of the patients with moderate or serious hemiplegia, and most of those with motor disorders show functional recovery on discharge.
Finally, these patients can manage by themselves with their daily life activities, with clear sensorium and walking adequately, though they show some limitation in the affected extremity.
Any disorder that persists after six months will be probably permanent. The recurrence after the cerebral infarction is frequent, worsening further the neurological sequels.
Non-elderly age, sensory and motor disorders alone, integer mental function and a collaborating environment at home enhance a good rehabilitation.
The patient and his relatives should understand the nature of the disability.
Physical and occupational therapy should focus on the use of the affected extremities, in order to achieve performing the basic functions, including driving.
Car adaptations are often necessary to allow for an adequate control of commands.
Mood changes can be the result of the infarction or a reaction to the situation. Tranquilizers and antidepressants are useful once the condition of the patient has stabilized.
Advice on stroke in progress and established
In a large number of patients driving is not recommended after a cerebral infarction, for the permanent, disabling sequels.
Physical and occupational therapy should insist on the use of the affected extremities, in order to fulfill the basic functions including driving.
The patient who improves from the cerebral infarction to complete recovery, an uncommon situation, can drive again without restrictions if his physician thus indicates it.
Mild sequels can permit driving, but for this purpose adaptations in the car are necessary that assure the adequate control of the commands.
Drivers with a high risk of recurrence of the cerebral infarction cannot drive.
Driving is not permitted until the cause originating the cerebral infarction is diagnosed and the treatment is established and adjusted, even if the recovery has been complete and without symptoms.