left CN3, 4,5-1, or 6 palsy

NPC patient with left eye ocular motor palsy, left ptosis
dysarthria, dysphagia
chart 3716182

HACE vergetative resurection

青海高原
塊肉餘生
白菜復活
翠玉如新
the rate of ascend
the prevention recommendation

NE New York University School of Medicine

The Precise Neurological Exam

Previous Lesson | Home | Next Lesson

General Appearance
Have the patient sit facing you on the examining table. Take a few seconds to actively observe the patient, and continue to actively observe the patient during the exam.

Level of consciousness. Always begin the exam by introducing yourself to the patient as a tool to evaluate the patient's gross level of consciousness. Is the patient awake, alert and responsive? If not, then the exam may have to be abbreviated or urgent actions may have to be taken.

Personal Hygiene and Dress.
Note the patient's dress. Is it appropriate for the environment, temperature, age or social status of the patient? Is the patient malodorous or disheveled?

Posture and Motor Activity. What posture does the patient assume when instructed to sit on the table? Are there signs of involuntary motor activity, including tremors (resting versus intention, also note the frequency in hertz of the tremor), choreoathetotic movements, fasciculations, muscle rigidity, restlessness, dystonia or early signs of tardive dyskinesia? Chorea refers to sudden, ballistic movements, and athetosis refers to writhing, repetitive movements. Fasciculations are fine twitching of individual muscle bundles, most easily noted on the tongue. Dystonia refers to sudden tonic contractions of the muscles of the tongue, neck (torticollis), back (opisthotonos), mouth, or eyes (oculogyric crisis). Early signs of tardive dyskinesia are lip smacking, chewing, or teeth grinding. Damage to the substantia nigra may produce a resting tremor. This tremor is prominent at rest and characteristically abates during volitional movement and sleep. Damage to the cerebellum may produce a volitional or action tremor that usually worsens with movement of the affected limb. Spinal cord damage may also produce a tremor, but these tremors do not follow a typical pattern and are not useful in localizing lesions to the spinal cord.

Height, Build and Weight.
Is the patient obese or cachectic? If cachectic, note any wasting of the temporalis muscles. Note the general body proportions and look for any gross deformities. Also check for dysmorphic features, including low set ears, wide set eyes, small mandible, mongoloid facies, etc.

Vital Signs.
These include temperature, pulse, respiratory rate and blood pressure. It is essential that the vitals always be taken as an initial assessment of a patient. Emergency measures may have to be taken for drastically abnormal vital signs.

Follow this vital sign acquisition routine:

Place the thermometer under the patient's tongue and instruct the patient to keep it there. Wait 20-30 seconds for the results.

Next, find the radial pulse in the patient's right arm with your first two fingertips of your right hand. Look at your watch and count the pulses over 15 seconds and then multiply by 4. Note the quality of the pulse. Is it bounding or thready, weak or prominent, regular or irregular, slow or rapid?. Once you are finished with the pulse measurement, keep your fingers on the pulse and secretly look at the patient's chest and count respirations for 15 seconds and also multiply this number by 4. Keeping your hand on the patient's pulse prevents the patient from becoming conscious of you watching them breath, preventing a likely adjustment in their respiratory rate.

Next, take the blood pressure. If it is high repeat the measurement later in the examination.

Finally, if a high temperature is present, or a previous history was taken suggesting meningeal irritation, test the patient for meningismus. Ask the patient to touch their chin to their chest to evaluate neck stiffness (a person with meningeal inflammation can only do this with pain). A positive Brudzinski's test is when the patient lifts their legs off the table in an effort to releave pain felt when the neck is flexed.

Next, have the patient lie flat on the examining table. Keeping the lower leg flexed, raise the upper leg until it is perpendicular to the floor. Slowly extend the lower leg while keeping the upper leg stationary. If meningeal irritation is present, this maneuver will be painful for the patient. Sometimes the patient will raise their head off the table and/or scream if pain is present, this is considered a positive Kernig's test. Meningismus consists of fever, clouding of consciousness, photophobia (bright light being painful to look at), nuchal rigidity, a positive Brudzinski's test, and possibly a positive Kernig's test.

Special Topic: Classic Cerebrospinal Fluid Characteristics

Idiopathic Seizures	Clear CSF with normal protein, normal glucose, no WBC's, no RBC's, normal opening pressure and normal % Gamma globulin.
Bacterial Meningitis:	Milky CSF with increased protein, decreased glucose, high WBC's (PMN predominate), few RBC's, mildly increased opening pressure and normal % Gamma globulin.
Guillain-Barre Syndrome:	Yellow CSF with very high protein (up to a gram), normal glucose, no WBC's, no RBC's, normal opening pressure and normal % Gamma globulin.
Subarachnoid Hemorrhage:	Yellow CSF with increased protein, normal glucose, few WBC's, inumerable RBC's, mildly increased opening pressure and normal % Gamma globulin.
Herpes Simplex Encephalitis:	Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominate), few RBC's, increase in opening pressure and normal % Gamma globulin.
Viral Meningitis:	Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominate), no RBC's, normal opening pressure and normal % Gamma globulin.
Multiple Sclerosis:	Clear CSF with mild increase in protein, normal glucose, few WBC's (lymphocytic predominate), no RBC's, normal opening pressure, increased % Gamma globulin.
Benign Intracranial Hypertension:	Clear CSF with normal protein, normal glucose, no WBC's, no RBC's, increased opening pressure and normal % Gamma globulin.

---

Previous Lesson | Home | Next Lesson

©1995-2006 New York University School of Medicine
Questions or comments?

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.

page 2025

page 2026

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　

seizure or Adam-Stokes attack due to hypoxia

3258352 06C 09 01 7o male laryngeal cancer transfer to 4FI 06
Stokes-Adams attackWikipedia, the free encyclopedia - Cite This SourceThe term Stokes-Adams Attack refers to a sudden, transient episode of syncope, occasionally featuring seizures. It is named after two Irish physicians, Robert Adams (1791–1875) and William Stokes (1804–1877).
Signs and symptomsThe patient goes pale just before the attack, the pulse stops, and they collapse. Normal periods of unconsciousness are around 30 seconds; if seizures are present, they will consist of twitching after 15–20 seconds. Breathing continues normally throughout the attack, and so on recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.
As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient's position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.
DiagnosisStokes-Adams attacks may be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic. The ECG will show asystole or ventricular fibrillation during the attacks.
CausesThe attacks are caused by loss of cardiac output due to cardiac asystole, heart block, or ventricular fibrillation. The resulting lack of blood flow to the brain is responsible for the faint.
TreatmentTreatment is normally surgical, involving the insertion of a pacemaker.
PrognosisIf undiagnosed (or untreated), Stokes-Adams attacks have a 50% mortality within a year of the first episode. The prognosis following treatment is very good.
Wikipedia, the free encyclopedia © 2001-2006 Wikipedia contributors (Disclaimer)This article is licensed under the GNU Free Documentation License.Last updated on Sunday May 06, 2007 at 04:33:34 PDT (GMT -0700)View this article at Wikipedia.org - Edit this article at Wikipedia.org - Donate to the Wikimedia Foundation