Q I’ve just had what my doctors call a ‘transient ischaemic attack, or TIA. For about 20 minutes, my sight blurred and dimmed, and I lost my hearing and ability to speak. My hands also began to go numb. As I had to wait several hours at the hospital, by the time a doctor saw me, I had no symptoms.
More than 10 years ago, I had two similar episodes, each about two years apart, but a load of tests, including an MRI scan, could find nothing wrong.
These episodes never occurred before I contracted Lyme disease 12 years ago. A year after that, I had my first attack. Since then, I have had an irregular and rapid heartbeat, and I am susceptible to everything going, including every type of flu.
Before the TIA, my doctor wanted to put me on beta-blockers to regulate my heartbeat but, according to tests, my heart is fine. He believes there is no imminent danger of a stroke as I have no family history of it, although my grandmother did have a stroke at age 26.
I don’t have high blood pressure or drink and, at 33, I’m probably too young for hardened arteries. My only other symptom is general fatigue, which means I often live on coffee. What should I do?- MM, Maidstone
A Transient ischaemic attacks are mini-strokes, when the blood supply to parts of the brain is temporarily interrupted or blocked. A stroke can be due to lack of blood (thus lack of oxygen) to the brain which, in turn, is caused by atherosclerosis, a ruptured blood vessel or a blood clot from elsewhere in the body which travels to the brain. During a proper stroke, there is brain damage and even death.
While stroke damage can persist for weeks or permanently, a TIA lasts only a few minutes or, at most, an hour, and there is no permanent damage.
It’s a shame you weren’t seen promptly as you need to be medically evaluated within 60 minutes of the attack to determine whether you suffered a genuine stroke or only a TIA.
In our view, your doctor is remiss in dismissing TIAs as just part of your makeup, a typical and now outdated attitude. In a new study (J Am Med Assoc, 2000; 284: 2901-6), only 14 per cent of patients with TIAs were hospitalised and 8 per cent received no subsequent treatment whatsoever to protect them from a serious stroke later.
TIAs should be considered a major warning of a future full-blown stroke, and all possible causes should be ruled out. The same study showed that 10 per cent of those who had TIAs went on to have a major stroke within the next 90 days. Indeed, half the strokes occurred within two days of the TIA.
This makes it imperative that your doctor run the gamut of routine tests on you as a matter of urgency to find out if your episode had any cause – a blockage, clot or haemorrhage – which could lead to a full-blown stroke later. These tests include Doppler ultrasound of your carotids (the neck arteries feeding blood to the brain) and other arteries to see if there is any minor or major blockage. Often, in stroke, both arteriosclerosis (hardened arteries) and arterial occlusions (clots) are present since platelet thickening may occur due to a damaged arterial lining. You should also undergo all the usual tests to determine your risk of stroke.
You also need to check your blood pressure, as high blood pressure can sometimes lead to an aneurysm, where a section of the arterial wall balloons out and bursts, causing a haemorrhage in the brain.
In a sense, you were lucky to have the TIA before taking beta-blockers, as these are just one of a large number of drugs which can cause a stroke in susceptible individuals. Others include sumatriptan, taken for migraines (Intensive Care Med, 1995; 21: 82-3); all hormones, including HRT and the Pill (Acta Neurol Belg, 1992; 92: 45-7); phenylpropanolamine, present in OTC drugs for weight loss, cold preparations and nasal decongestants (Am J Emerg Med, 1987; 5: 163-4); nifedipine, a calcium-antagonist type of antihypertensive (BMJ, 1992; 305: 693); and any sort of nasal decongestants used excessively (J Neurol Neurosurg Psychiatry, 1989; 52: 541-3). Ironically, even drugs used to prevent stroke – such as anticoagulants, streptokinase, heparin and recombinant tissue-type plasminogen activators – can cause a stroke (Circulation, 1991; 83: 448-59; Arch Neurol, 1985; 42: 1033-5).
Even thrombolytics, the drugs used to dissolve blood clots after a cerebral infarction, or blockage of a vessel in the brain, can bring on another stroke – this time, by haemorrhage.
We’re frankly mystified at the suggestion to take beta-blockers for a rapid heartbeat. Certain beta-blockers, like Sotacor, can cause torsade de pointes, or an unusually rapid heartbeat of more than 100 beats per minute, according to Sortacor’s manufacturer, Bristol-Myers Squibb (Physicians’ Desk Reference).
So if you are taking any sort of medication, even for migraine, you might consider this a possible cause of your TIAs.
Ordinarily, if there are one or more risk factors for stroke, a doctor may suggest either drug therapy or surgery to reduce your risk. The gold standard of preventative stroke therapy is antiplatelet therapy – taking aspirin. Aspirin supposedly ‘works’ by thinning the blood and lowering blood pressure, and is a first-line treatment for TIA patients. The bottom line is that aspirin has never been proven to prevent stroke in low-risk patients with no history of cardiovascular disease (N Engl J Med, 1992; 327; 175-81).
Furthermore, aspirin is given in daily dosages of 5-325 mg/day but, at this level, it can act paradoxically – by increasing the risk of a burst blood vessel in the brain by 21 per cent, even in low-risk patients (Drugs Ther Bull, 1994; 32: 1 – 3).
One of the problems in using long-term just-in-case medicine like aspirin is that it depletes the body of many vital nutrients, which may be essential for protecting your heart and blood vessels.
In a study comparing patients taking aspirin with those taking warfarin and still others left untreated, there was no significant difference in low-risk patients between doing something and doing nothing; in high-risk patients, the differences between the three groups were large enough to be statistically significant, but not enough to be meaningful in terms of survival (J Am Med Assoc, 1995; 274: 1839-45).
The only other usual treatment for stroke is an operation to scrape away fatty deposits in your carotid arteries, which is unlikely in your case, given your age.
>From what you say, you don’t have any of the obvious causes for a TIA – high cholesterol, smoking, diabetes or alcohol abuse – although with your grandmother’s circumstance, there is a possibility of a genetic propensity to stroke.
Although you don’t give much information about your general health, one detail is highly significant: you had Lyme disease, caused by a bite from a tick which spreads Borrelia burgdorferi, a spiral-shaped bacteria). Although this disease is most prevalent in the US, it is being seen in increasing numbers in the UK. If left untreated, symptoms can come and go for years.
Numerous studies show that untreated Lyme disease can cause different neurological problems that imitate true stroke and TIAs. Indeed, the evidence suggests that Lyme borreliosis may be a more common cause of these puzzling episodes than medicine has previously thought.
In a study of patients with cerebral thrombosis or TIAs without a thrombosis, 24 of the 281 patients – nearly 9 per cent – had an immune-system response to B. burgdorferi, suggesting the presence of the bacteria in their blood. The researchers concluded that the symptoms of Lyme borreliosis may often masquerade as stroke (Stroke, 1993; 24: 1393-6).
Your tachycardia (rapid heartbeat) may also be related to Lyme myocarditis (heart inflammation due to the Lyme spirochaete) rather than a structural problem. In one case study, Lyme myocarditis had all the hallmarks of tachycardia (J Cardiovasc Electrophysiol, 1997; 8: 323-4).
Animal studies have shown that B. burgdorferi has a predilection for cardiac connective tissue, especially near the aorta (Am J Trop Med Hyg, 1992; 47: 249-58).
Carditis is seen in 4-10 per cent of all cases of Lyme disease. Its symptoms usually include various types of atrioventricular block, or abnormalities in the electrical conduction tissue between the chambers of the heart, leading to disturbances in heart rhythm if left untreated (Ugeskr Laeger, 1993; 155: 2147-50).
In some cases, a pacemaker may be necessary (J Cardiovasc Electrophysiol, 1997; 8: 323-4). According to the researchers of one study, when serious arrhythmias are present and a cause can’t be found, Lyme disease should be one of the first possibilities considered, particularly among young people (Ugeskr Laeger, 1993; 155: 2147-50).
Although Lyme disease is often difficult to diagnose and treat, aggressive treatment with a strong antibiotic like ceftriaxone can often do the job. In six patients with Lyme carditis treated with antibiotics, echocardiograms and exercise tests showed that symptoms resolved up to seven years after the acute disease (Scand J Infect Dis, 1997; 29: 153-7). There is controversy over whether a short- or long-term course of antibiotics will truly kill this intractable bug (see WDDTY, vol 12 no 3) and also whether it can be completely eradicated after being in the system for so long – in your case, 12 years.
There is increasing evidence that colloidal silver is effective against B. burgdorferi. You may also wish to augment any type of antimicrobial treatment with vitamins and minerals that counter heart disease and stroke; this includes consuming a wholegrain diet rich in fruits and vegetables, supplementing with magnesium, coenzyme Q10 and antioxidants, and taking regular exercise. Just taking regular supplements of vitamin E, for instance, can decrease blood platelet stickiness by 80 per cent (Blood, 1989; 73; 141-9).