Transient Focal Neurological Events

Transient Ischemic Attacks

A TIA is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction . In past years TIAs were arbitrarily characterized as lasting less than 24 h. Modern brain and vascular imaging showed that ischemic attacks that lasted longer than 1 h were most often associated with brain infarction. Most TIAs last less than 1 h.

Seizures

Seizures account for up to 38% of TIA-stroke mimics . Risk factors for seizures include prior strokes, small vessel disease, head injuries, brain tumors, subdural hematomas (SDHs), vascular malformations, and space-occupying lesions. Patients can present in any stage of the seizure or postictal period; initial ictal symptoms or signs may be unwitnessed or subtle and can go unrecognized by the patient (particularly in those who have cognitive impairment) and medical professionals. Presentation is highly variable depending on the seizure focus, both with regard to ictal and postictal symptoms as well as the duration of symptoms.

During the ictal phase, spontaneous neuronal discharge most often leads to positive phenomena including focal or generalized limb jerking or myoclonic jerks and positive sensory symptoms such as paresthesias or simple positive visual phenomena such as bright colors or flashes of light. Positive phenomena are less common in patients who have TIAs. Frequent epileptiform discharges can also interrupt speech and thought processes resulting in brief periods of speech arrest or aphasia at times with florid paraphasic errors. Postictally, there is cortical suppression resulting in negative symptoms and signs such as weakness, numbness, or speech difficulty. The classical Todd’s paresis, which often presents with hemiparesis, occurs commonly after generalized tonic-clonic or focal motor seizures . The duration of postictal dysfunction may last for days or longer. A clue to a convulsive etiology is the tempo of onset, which evolves rapidly over several seconds with spreading focal involvement or secondary generalization. This allows differentiation from the much slower progression seen in migraine or the classically abrupt onset seen in stroke. A reduced level of consciousness is also more common in seizures than in TIAs. Electroencephalography can be used to identify epileptiform discharges. When attacks similar to the presenting event have occurred for years, seizures and migraine are more likely than stroke. Hyperperfusion seen in patients with seizures on computed tomography (CT) or MRI-perfusion imaging may be helpful and different from the pattern found in stroke .

Migraine

Migraine is a very common TIA mimic. The incidence of migraine declines with age, but it is still relatively frequent in the older population . A thorough history is important to detail the progression of symptoms and neurological deficits as well as the co-occurrence of a migrainous sounding headache. In comparison with the sudden onset symptoms in stroke and very rapid spread in seizures, migraine auras have a characteristic, slow spread during several minutes due to cortical spreading depression . The sensory symptoms typically begin with positive signs that can involve different sensory modalities. Patients may have headache before, during, or after the episode. Often, the first symptoms are a positive visual aura, a sensation of fluttering, bright flashes of light, scintillations, shimmering, or a change in perspective. A migrainous visual aura is often characterized by gradual movement across the visual field leaving behind in its trail negative phenomenon in the form of an area of decreased vision that slowly resolves. In patients with stroke, there is no clear spread and involvement is in only one visual field as opposed to bilaterally in migraines and does not spread. The “scintillating scotoma,” a combination of both negative and positive phenomena seen in migraine, is not seen in other conditions. When the visual symptoms clear, another positive phenomenon in the form of a tactile sensory aura may begin. Paresthesias most often involve the hand and face with legs and torso much less commonly affected. The sensation can be described as tingling, prickling, or burning sensations. The abnormal sensation starts focally, whether in a finger or leg, or on the face and will slowly evolve and may even spread to the contralateral side. This nonanatomic distribution also provides an additional clue that the symptoms do not respect the focal anatomic confines seen in strokes. The sensory aura resolves slowly, with the first affected area clearing last and often leaves behind a feeling of decreased sensation in its wake. As these positive symptoms recede, patients may then develop other “negative” symptoms such as weakness, aphasia, or other problems. Aphasic auras generally involve paraphasic errors in addition to word-finding difficulties. Associated weakness is generally slight in comparison with cerebrovascular causes and has a rostrocaudal typical sensory march. Patients with a clear history of migraine or prior migrainous sounding headaches with aura have an increased likelihood of an atypical migrainous aura particularly if there is a history of previous complex features.

Migrainous aura without headache, now termed acephalgic migraine, was first described in Miler Fisher’s classic paper where he detailed migraine accompaniments in individuals above age 45 years, most often in the absence of headache . Migraine accompaniments involving sensory, motor, and aphasic symptoms almost always co-occur with a visual aura. Table 76.1 details features distinguishing migraine accompaniments from TIA.

A particularly challenging mimic at any age is migraine with brainstem aura . Onset is most common in youth but there are late-onset cases. The onset is most often visual that can have both positive or negative features and other symptoms localizable to the brainstem including slurred speech, vertigo, tinnitus, hypacusis, diplopia and oscillopsia, and gait and appendicular ataxia. Patients may also report paresthesias in the perioral region or in the limbs and some may also have decreased consciousness. Examination is highly variable and may reveal ophthalmoplegia, ataxia, dysarthria, or other cranial nerve abnormalities.

Transient Global Amnesia

Transient global amnesia (TGA) usually occurs in older age and is characterized by the sudden onset of profound anterograde amnesia with more variable retrograde memory loss, followed by a gradual recovery, which may last several hours and almost always less than 24 h . Most cases are single events, although some patients have recurrent attacks. Patients appear confused, and invariably ask repetitive questions about why they are here and sometimes where they are. They are unable to retain information given to them. Patients may be anxious and can be agitated, although some become quiet and withdrawn. Despite the dramatic memory loss and disorientation to place and time, patients have otherwise intact cognitive function and no other neurological symptoms. They may be able to drive safely, calculate, play a musical instrument, or even deliver a speech. Following resolution of symptoms, there is permanent memory loss for the events during the attack. Caplan produced a set of criteria for TGA that was later refined by Hodges and Warlow ( Table 76.2 ) :

TGA is associated with physical, sudden, or unexpected psychological stress as well as positive emotional responses; funerals as well as celebrations have been temporally related. Most patients endorse precipitating events that include recent sexual activity, physical exertion, swimming in cold water (“amnesia by the sea”), a hot bath, or shower . These triggering events are similar to those of migraineurs. Patients may have a past history of migraine .