Brainstem stroke and fusiform aneurysm of veterbrobasial arteries

2007/07/16 ER consulation
M79 96.07.16 14:07 張oo 56 man (chart 4351731)
diplopia for 3 days, unsteady gait with deviation to the right side
VB fusiform aneurysm related brainstem stroke
how to manage this case?

Neurological Disorders and Sleep Disturbance

Neurological Disorders and Sleep Disturbance

Sleep disorders are very common in neurological illnesses, which may adversely affect patients' sleep. Thus there is an interrelationship between sleep and neurological disorders. Sleep dysfunction may result from central or peripheral somatic and autonomic neurological disorders. Neurological diseases may cause insomnia or EDS as well as parasomnias. Neurological causes of excessive sleepiness have been described previously, and neurological disorders that cause insomnia are described under Insomnia, earlier in this chapter.

Sleep and Epilepsy

There is a distinct and reciprocal relationship between sleep and epilepsy (Chokroverty and Quinto 1999; Dinner 2002). Sleep affects epilepsy, and epilepsy affects sleep. In the beginning of the last century, before the availability of encephalography, several authors emphasized that many seizures are predominantly nocturnal and occur at certain times at night. The modern era of combining the clinical and EEG findings on sleep and seizures began with the observation of Gibbs and Gibbs in 1947 that EEG epileptiform discharges were seen more often during sleep than during wakefulness (Chokroverty and Quinto 1999). A basic understanding of the mechanism of epileptogenesis and sleep makes it clear why seizures are often triggered by sleep. The fundamental mechanism for epileptogenesis includes neuronal synchronization, neuronal hyperexcitability, and a lack of inhibitory mechanism. During NREM sleep, there is an excessive diffuse cortical synchronization mediated by the thalamocortical input, whereas during REM sleep, there is inhibition of the thalamocortical synchronizing influence in addition to a tonic reduction in the interhemispheric impulse traffic through the corpus callosum. Factors that enhance synchronization are conducive to active ictal precipitation in susceptible individuals. NREM sleep thus acts as a convulsant by causing excessive synchronization and activation of seizures in an already hyperexcitable cortex. In contrast, during REM sleep, there is attenuation of epileptiform discharges and limitation of propagation of generalized epileptiform discharges to a focal area.

Sleep deprivation is another important seizure-triggering factor, and the value of sleep-deprived EEG studies in the diagnosis of seizures is well known. Sleep deprivation increases epileptiform discharges, mostly during the transition period between waking and light sleep. Sleep deprivation causes sleepiness, which is one factor for activation of seizures, but it probably also increases cortical excitability, which triggers seizures. However, in a recent report on 84 patients with medically refractory partial epilepsy with secondary generalization undergoing inpatient monitoring, Malow et al. (2002) noted that acute sleep deprivation did not affect seizure incidence.

Biorhythmic classification of seizures has shown inconsistencies and contradictions. Seizures have been shown to occur predominantly during sleep (nocturnal seizures), predominantly in the daytime (diurnal seizures), or both during sleep at night and daytime (diffuse epilepsy). Taking into consideration different series, the incidence of sleep epilepsy has been quoted to be 22%, but most of these statistics were obtained before the advent of electroencephalography. The most likely figure for nocturnal seizures is about 10%. Because of inconsistencies in biorhythmic classification, modern epileptologists use the International Classification of Epilepsy, which divides seizures into primarily generalized and partial seizures with or without secondary generalization.

Effect of Sleep on Epilepsy.

True nocturnal seizures (Malow and Plazzi 2003; Chokroverty and Quinto 1999) may include tonic seizures, benign focal epilepsy of childhood with rolandic spikes or occipital paroxysms, juvenile myoclonic epilepsy, electrical status epilepticus during sleep or continuous spikes and waves during sleep, generalized tonic-clonic seizures on awakening, nocturnal frontal lobe epilepsy including nocturnal paroxysmal dystonia (NPD), and a subset of patients with temporal lobe epilepsy (nocturnal temporal lobe epilepsy). Many patients with generalized tonic-clonic and partial complex seizures also have predominantly nocturnal seizures. Nocturnal seizures may be mistaken for motor and behavioral parasomnias or other movement disorders that persist during sleep or reactivate during stage transition or awakenings in the middle of the night.

Tonic Seizure.

Tonic seizures are characteristic of Lennox-Gastaut syndrome, which may also include other seizure types, such as myoclonic, generalized tonic-clonic, atonic, and atypical absence. Tonic seizures are typically activated by sleep, occur much more often during NREM sleep than during wakefulness, and are never seen during REM sleep. The typical EEG finding consists of slow spikes and waves intermixed with trains of fast spikes as interictal abnormalities during sleep.

Benign Rolandic Seizure.

Benign rolandic seizure is a childhood seizure disorder seen mostly during drowsiness and NREM sleep and is characterized by focal clonic facial twitching, often preceded by perioral numbness. Many patients may have secondary generalized tonic-clonic seizures. The characteristic EEG finding consists of centrotemporal or rolandic spikes or sharp waves and sometimes occipital spikes. Seizures generally stop by the 15-20 years of age without any neurological sequela.

Juvenile Myoclonic Epilepsy.

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Onset of myoclonic epilepsy of Janz usually occurs between 13 and 19 years of age and is manifested by massive bilaterally synchronous myoclonic jerks. The seizures increase shortly after awakening in the morning and occasionally on awakening in the middle of the night. A typical electroencephalogram shows synchronous and symmetrical polyspikes and spike-and-wave discharges. The interictal discharges predominate at sleep onset and then on awakening but are virtually nonexistent during the rest of the sleep cycle.

Nocturnal Frontal Lobe Epilepsy.

Nocturnal frontal lobe epilepsy includes (Provini et al. 1999; Malow and Plazzi 2003) nocturnal paroxysmal dystonia, paroxysmal arousals and awakenings, episodic nocturnal wanderings, and autosomal dominant nocturnal frontal lobe epilepsy. These disorders all share common features of abnormal paroxysmal motor activities during sleep and respond favorably to anticonvulsants. They most likely represent partial seizures arising from discharging foci in the deeper regions of the brain, particularly the frontal cortex, without any concomitant scalp EEG evidence of epileptiform activities. The relationship to seizures, particularly partial complex seizures of temporal or extratemporal origin, however, remains controversial. Nonepileptic seizures or pseudoseizures are not common during sleep at night but sometimes can occur and be mistaken for true nocturnal seizures, and it is important to differentiate these from true seizures because of difference in management.

Table 74-22. Features of nocturnal paroxysmal dystonia

Onset: infancy to fifth decade

Usually sporadic; rarely familial

Sudden onset from non-rapid eye movement sleep

Two clinical types: Common type is short-lasting (15 sec to <2>

Semiology: ballismic, choreoathetotic, or dystonic movements

Often occurs in clusters

Electroencephalogram: generally normal

Short-duration attacks are most likely a type of frontal lobe seizure

Treatment: carbamazepine effective in patients with short-lasting attacks

Table 74-23. Features of frontal lobe seizures

Age of onset: infancy to middle age

Sporadic, occasionally familial (dominant)

Both diurnal and nocturnal spells, sometimes exclusively nocturnal

Sudden onset in non-rapid eye movement sleep with sudden termination

Duration: mostly less than 1 min, sometimes 1-2 min with short postictal confusion

Often occur in clusters

Semiology: tonic, clonic, bipedal, bimanual, and bicycling movements; motor and sexual automatisms; contralateral dystonic posturing or arm abduction with or without eye deviation

Ictal EEG may be normal; interictal EEG may show spikes; sometimes depth recording is needed

	EEG = electroencephalogram.

Five patients were originally described who had episodes of abnormal movements that were tonic and often violent during NREM sleep almost every night. Ictal and interictal EEG findings were normal. Later, 12 patients were described with NREM sleep-related choreoathetotic, dystonic, and ballismic movements each night, often occurring many times during the night for many years. The term nocturnal paroxysmal dystonia (NPD) was coined for this entity (Table 74.22). The disorder in all patients responded to carbamazepine therapy, and the spells lasted less than 1 minute. It was suggested that these spells were a type of unusual nocturnal seizure. Later, patients with NPD showed EEG evidence of epileptiform abnormalities arising from the frontal lobes. A study comparing groups of patients with NPD and those with undisputed frontal lobe seizures supported the contention that patients with NPD may have frontal lobe seizures. Therefore, short-duration NPD attacks may represent a form of frontal lobe seizures (Table 74.23) that are evoked specifically during sleep at night. Provini and co-workers (1999) gave a comprehensive review of clinical and EEG features of 100 consecutive cases of nocturnal frontal lobe epilepsy.

Autosomal Dominant Nocturnal Frontal Lobe Epilepsy.

An autosomal dominant form of frontal lobe epilepsy usually starts in childhood and persists throughout adult life. Attacks are characterized by brief motor seizures in clusters during sleep. Neurological examination and neuroimaging studies are normal. Videotelemetry during the attacks confirms their epileptic nature, and the response to carbamazepine treatment is excellent (Scheffer et al. 1995).

Effect of Epilepsy on Sleep

Although the usefulness of sleep in the diagnosis of epilepsy has been established, the altered sleep characteristics in epileptic patients are not well known. Most studies have been conducted in patients who have been receiving anticonvulsants, thus adding the confounding factors of the effect of anticonvulsants on sleep architecture. Additionally, there is a dearth of longitudinal studies to determine the effect of epilepsy on sleep in the early stage versus the late stage of illness. A general consensus has been reached, however, on the effects of epilepsy on sleep and sleep structure. These effects can be summarized as follows: an increase of sleep-onset latency; an increase in waking after sleep onset; a reduction in REM sleep; increased instability of sleep states, such as unclassifiable sleep epochs; an increase in stages I and II NREM sleep; a decrease in stages III and IV NREM sleep; and a reduction in the density of sleep spindles.

Printed from: Neurology in Clinical Practice (on 11 July 2007) © 2007 Elsevier

IV fluid administration in ischemic stroke for a CHF old-aged patient

2007/7/7 ICU work all night due to a large infarction of the right MCA territory in a patient with CAD 3-V-D s/p POBAS, CHF s/p pacemaker,

04D1-01-01　林OO 　2212815　M　民國 19.02.02

be careful in IV orders because of old age with CHF
keep I/O balance and monitor very closely