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Transcript
EPISODIC EVENTS: VIDEO CASE EXAMPLES
Jessica Schmidt, DVM, DACVIM (Neurology)
Wheat Ridge Animal Hospital
INTRODUCTION
An episode is defined as something an animal does that the client witnesses and is over by the time the pet is presented for
our evaluation. The client's ability to convey what transpired is frequently clouded by the fear and anxiety they experienced during the
episode. Henceforth, what they describe may be somewhat disorganized, abbreviated and lacking valuable information. We can make
an effort to circumvent this by focusing the client on what the pet was doing prior to, during, as it was coming out of, right after and in
between the episodes (inter-episode). Asking questions to help clarify the events and comparing the clients’ description to your
mental images of the different causes of episodes will help you either conclude or narrow down the possible considerations.
Addressing issues about the animal’s mental status, eye movements, ability to move, gait change, head, limb and body posture,
evidence of pain, autonomic release, respiratory patterns and mucus membrane color are all important. The differential diagnosis of
an episode includes seizure, syncope, stroke, encephalopathy, increased intracranial pressure, vestibular, narcolepsy, weakness, pain,
tremor and behavioral. One should not have tunnel vision and jump to specific conclusions without good reason. Until confident
enough to call it otherwise, the event should be labeled an episode.
SEIZURE
A seizure is a paroxysmal electrical dysrhythmia of the brain, which begins abruptly, frequently ceases spontaneously and
has a tendency to reoccur. Depending on the area of brain discharging, seizures can be subdivided into major motor, focal motor or
complex motor. Manifestations of the convulsive phase (or ictus) of major motor seizures include a mentation change, purposeless
limb movements, salivation, urination and defecation usually lasting for 30 seconds to several minutes. This is followed by a post-ictal
period up to 24 hours long and characterized by changes in behavior, intellect, personality and habits. Major motor seizures
frequently occur when a pet is at rest or sleeping but may be precipitated by excitement, anxiety, flashing lights, feeding, etc. Focal
motor seizures result in face, limb or trunkal twitching or jerking (dysryhthmic) movements that often cause the animal to fall or
nearly fall. Complex motor seizures (limbic lobe or psychomotor epilepsy) is characterized by repetitive motor activity which may
include fly biting, floor licking, tail chasing, pounce-prey activity, excessive swallowing with regurgitation and even aggression. The
causes of major and focal motor seizures can be divided into systemic diseases and primary intracranial disorders. Potential systemic
causes of major and focal motor seizures include exposure to certain substances (i.e. lead, organophosphate, medication/drug
overdose), hypoglycemia or hypocalcemia, liver or kidney disease, circulatory problems (i.e. hypertension, hyperlipidemia,
hyperviscosity), coagulation disorders and hormonal imbalances (i.e. hypo- or hyper-thyroidism, hyperadrenocorticism). Extensional
brain infection and tumor, encephalitis, hydrocephalus, trauma, primary or metastatic brain tumor, rarely storage diseases and not
infrequently idiopathic are differential intracranial considerations. Most cases of complex partial seizures are idiopathic. Diagnostic
and treatment recommendations are based on signalment, neurologic exam abnormalities, and evidence of systemic signs of illness
and seizure severity.
SYNCOPE
Syncope is characterized by a sudden loss of consciousness, alteration of limb function, pallor or cyanosis (which may not be
recognized by the client) and sometimes evacuation of urine. The event is frequently precipitated by exercise, excitement or
coughing. It may last up to 30 seconds and the pet usually recovers quickly without a definable period of disorientation. Inter-episode
the pet may demonstrate coughing, labored breathing and fatigue while physical exam may reveal cardiac arrhythmia and pulse
deficits, murmur, abnormal lung sounds or respirations. It results from global brain ischemia due to a variety of cardiopulmonary
disorders. A thorough evaluation including ECG, thoracic radiograph, Doppler blood pressure, and possibly echocardiogram should be
performed when there is any doubt that an episode may be syncope. Halter or event monitoring can be an invaluable aid in capturing a
life threatening arrhythmia at the time of the attack. Erroneous conclusion of seizure in a syncopal patient and institution of
antiepileptic therapy could put the animal at serious risk of decompensation.
STROKE
A stroke or vascular accident typically results in a peracute onset of uncontrollable limb movements, muscle tone and
changes in body and head posture. Strokes can be difficult to differentiate from seizures and when a vascular episode resembles a
seizure it has been termed apoplexy. The pet may be active or at rest just prior to this episode. The hallmark of a vascular episode is a
peracute onset of lateralizing deficits, which requires evaluation of a complete neurologic exam. These deficits may be evident at the
time of the neurologic exam or they may resolve within minutes to hours, so it is important to question clients about any asymmetry of
head, limb or body posture and movements that may have been evident during the episode or as the pet is recovering. When the
lateralizing deficits resolve before the neurologic exam a stroke can be sub-categorized as a Transient Ischemic Attack (TIA). Interepisode abnormalities may pertain to signs related to the underlying systemic disease responsible for the stroke. Any disease which
causes hemorrhage, thrombosis, embolism or infarction of either the brain or spinal cord can result in a stroke. As with seizures, the
etiology of stroke can be divided into extra- and intra-cranial disorders. Systemic considerations include coagulopathy, hypertension,
hypothyroidism, Diabetes Mellitus, hyperadrenocorticism, glomerulonephropathy, pheochromocytoma and metastatic disease.
Primary CNS diseases include arteriovenous malformation, Feline Ischemic Encephalopathy and extensional tumors or infections that
compromise circulation. Laboratory tests ordered should be tailored to the patient signalment and physical exam findings. MRI is the
best imaging modality to make this diagnosis.
ENCEPHALOPATHY
Dysfunction of the brain that is associated with a spectrum of mentation changes ranging from hyperactivity and restlessness,
to reduced awareness and delirium, to dullness and decreased responsiveness. Signs are not typically exacerbated by any specific
activity but may be precipitated by eating (hepatic) or fasting (hypoglycemia). Frequently, these episodes do not have a clear-cut
beginning or end but typically are a continuum of worse periods with inter-episodic times of less profound abnormalcy that wax and
wane for hours or days before presentation. Inter-episodic signs of systemic disease (anorexia, lethargy, weight loss, pu/pd/pp, emesis,
etc.) would be supportive of this category of disease. The neurologic exam is often consistent with diffuse cerebral dysfunction
including a mentation change without evidence of lateralizing deficits. Etiologic considerations include toxic (substance abuse,
pharmaceutical preparations, lead, organophosphate) and metabolic (hepatic, hypoglycemia, renal, hyperosmolar, hyperviscosity,
hypothyroid) disorders. The client may or may not be aware of the pet ingesting toxic substances. Normal findings on CBC,
chemistry, T4, and pre and post-prandial bile acids are helpful in ruling out systemic disease. Treatment is specific to the underlying
disease.
VESTIBULAR
Episodes related to unilateral vestibular dysfunction are typically peracute in onset and characterized by listing, leaning,
veering, falling or rolling and frequently are accompanied by a head tilt. Bilateral disease will result in falling in both directions and
wide head excursions without a head tilt. Brief episodes of extensor rigidity and opisthotonus are not uncommon in pets with central
vestibular dysfunction. Episodes are frequently precipitated by activity because movement stresses the capacity of the vestibular
system leading to disequilibrium. Attacks most often last for days to weeks but may only last minutes to hours leaving the pet
apparently normal inter-episode. Nystagmus is frequently present during the episode but the client may not notice it and unless the
veterinarian looks for a positional nystagmus during the neurologic exam it may be missed. Vomiting is not unusual due to vertigo
stimulating the emetic center. Aside from being dysequilibric the pet has appropriate mentation, knowing where to go just having
trouble getting there. Cats fed all fish diets and those that are not eating well may display episodic central vestibular dysfunction from
thiamine deficiency. Chronic administration of Metronitazole to dogs may also result in vestibular dysfunction. Thyroid testing (i.e.
hypothyroid dogs, hyperthyroid cats) and blood pressure monitoring are important screening tests with vestibular disease. With
recurrent vestibular episodes, MRI or CT scan and CSF analysis should be considered to rule out underlying structural disease.
INCREASED INTRACRANIAL PRESSURE
Increased intracranial pressure (ICP) can result in episodic abnormalities of limb and postural tone. These episodes may be
precipitated by activity or situations that increase central venous pressure (coughing, defecation, jugular compression for
venipuncture). Signs can be related to midbrain compression and loss of inhibition of extensor tone to the head/neck, fore and rear
limbs (decerebrate rigidity); cerebellar compression and loss of inhibition to the extensors of the head/neck and forelimbs
(decerebellate rigidity); or irritative lesions of the vestibular nuclei resulting in central vestibular signs. The episode may last from
seconds to minutes. Decreased level of consciousness, pupillary asymmetry or decreased responsiveness and positional nystagmus are
not uncommon inter-episodic neurologic exam findings. The inter-episode neurologic exam may be normal. Increased ICP may result
from any pathologic process (mass, inflammatory, vascular, cyst, obstructive hydrocephalus) producing cytotoxic, interstitial or
vasogenic edema. The decision to perform a CSF tap should be postponed until after results of brain imaging because animals with
increased ICP are at greater risk of herniation with a CSF tap. If the increase pressure in the intracranial compartment is great enough
transtentorial or occipital foramen herniation may result. Administration of mannitol 2% @ 0.5-1gram/kg IV over 20 minutes and a
corticosteroid should be considered to reduce cerebral edema.
NARCOLEPSY/CATAPLEXY
The development of a sleep-like state or hypersomnolence (narcolepsy) frequently accompanied by flaccid paralysis of all
limbs (cataplexy). Eating, excitement, and playing most often precipitate these episodes. The episodes usually last seconds to
minutes but can last up to 30 minutes. Eye movements, muscular twitching and whining, as in REM sleep, may be evident. The pet
recovers quickly, completely and without aberrant behavior leaving them without inter-episodic neurologic exam abnormalities. A
hereditary basis has been demonstrated in many breeds of dogs. It tends to affect young adult dogs before 6 months of age. The
underlying pathogenesis is an alteration of CNS neurotransmitters, specifically hypoactive catecholaminergic, and hyperactive
cholinergic (M2 muscarinic) and dopaminergic2 in specific brain regions. Intravenous injection of yohimibine @ 25-50ug/kg will
result in a 90% reduction in the number of attacks from 20 minutes to 4 hours from the time of administration. The attack frequency
would have to be multiple per hour for this to be a valid test. More commonly, the response to yohimbine @ 50-100ug/kg PO every
8-12 hours or Imipramine @ 0.5-1.0mg/kg PO every 8 hours or Methylphenidate @ 5-10mg PO every 24 hours is evaluated.
WEAKNESS
Weakness is defined as a decreased (paresis) or inability (paralysis) to support weight against gravity or initiate movement.
Paresis is typically precipitated by exercise resulting in fatigue and collapse. Fatigue is characterized by a progressively stiffer, shortstrided gait and often-decreased ability to hold the head and neck up (ventral neck flexion). This type of gait disturbance is typically
reflective of neuromuscular disease. Inter-episodic historical cranial nerve involvement including decreased ability to blink, voice
change, stridor, dysphagia and/or regurgitation may be evident with some etiologies. The animal may be normal or only have subtle
evidence of a gait change, trouble rising, jumping or doing stairs inter-episode. Neurologic examination may reveal decreased
palpebral reflexes, diminished myotatic reflexes and generalized muscle atrophy. The patient, however, may have normal myotatic
reflexes and muscle mass despite fatigue, as is typically the case with Myasthenia Gravis. There are a host of systemic diseases (i.e.
hypokalemia, hypernatremia, hypothyroidism in dogs, hyperthyroidism in cats, hypoglycemia/hyperinsulism, paraneoplastic disease,
delayed OP toxicity) and primary neurologic disorders (cell body diseases, radiculopathies, neuropathies, junctionopathies,
myopathies) including immune, infectious, neoplastic and degenerative categories of disease that may result in neuromuscular
dysfunction. The administration of IV edrophonium chloride (Tensilon) @ 1-5mg/dog or 0.25mg/cat should be considered in a patient
with neuromuscular dysfunction or exercise associated collapse as it will result in an unequivocal improvement in strength when
consistent with a diagnosis of Myasthenia Gravis. Treatment of other conditions depends on results of laboratory tests and
electrodiagnostic procedures. Select laboratories should perform evaluation of peripheral nerve and muscle biopsies, as they require
special techniques in sample preparation and pathologists with advanced training in interpretation.
PAIN
Pain may take on an array of clinical signs that vary from overt vocalization to subtle posture changes to a host of behavior
changes that may or may not be consistent with what would typically be considered related to pain. Therefore, the possibility of pain
should always be considered and the client carefully questioned before ruling out this possibility. Another clinically important
principal is that you should be very cautious about concluding that an animal is in pain by results of your exam finding alone. Some
animals appear painful when they are merely overreacting to being manipulated. Alternatively, the absence of evidence of pain on
palpation should not be taken as an absolute indication the animal is not painful, that is, when the history or your observations are
suggestive of pain. Some animals are very stoic and do not demonstrate pain with our manipulation even when they do hurt.
Therefore, in either case, it is very important to place more emphasis on whether there is historical and observational evidence of pain
or discomfort based on vocalization, gait abnormalities or posture changes of the head, neck or back.
TREMOR
Tremors are rhythmic movements of the head, trunk or limbs. The body part moves with equal frequency at 180-degree
angle. These movements are evident when the pet is at rest and may be exacerbated by excitement or subside. They may last for
seconds to hours leaving the pet normal inter-episode. Differential considerations for tremors include toxins, neuromuscular disease
(electrolyte disorders, weakness, and demyelination), inflammatory CNS (“White Shaker” Disease) and degenerative disorders
(storage diseases). Episodic head tremors, common in certain breeds i.e. Dobermans and English bulldogs, may occur in a vertical
(“yes”) or horizontal (“no”) direction. The etiology is unknown but the head bobbing is more often benign. CBC, chemistry, T4
profile and bile acid response test are recommended to rule out underling disease. The use of distracters (i.e. peanut butter, toys,
exercise, etc.) to break the cycle is frequently effective. Phenobarbital has not been effective in head tremor cases severe enough to
warrant medication.
BEHAVIORAL
Behavioral categories of disease typically associated with episodes include aggression (i.e. dominance, fear, and territorial),
phobias (i.e. to noise, movement, separation) and obsessive-compulsive disease (i.e. tail chasing, excessive licking, barking or
drinking, pounce-prey activity). Differentiating behavioral aggression from that caused by complex seizures can be difficult on a
historical basis alone. If EEG is available it may reveal paroxysmal activity consistent with seizures. If not available, then a trial on
anticonvulsant would be a reasonable alternative. Repetitive motor activity can be a manifestation of OCD or complex seizures. The
habituation of a repetitive motor activity and its reoccurrence can be explained by the fact that the motor activity releases endorphins.
Henceforth, the cycle is perpetuated even if the repetitive activity causes self-injury (i.e. lick granuloma) and possibly pain. Behavior
modification and psychotropic drugs are the mainstays of therapy. It may take multiple, several week drug trials before one is proven
effective necessitating client education and patience.
CONCLUSION
Episodic disorders comprise an array of clinical presentations. Taking the time to get an accurate history is paramount to the
differential diagnosis and diagnostic recommendations. Failure to attempt to characterize the episodes may lead to performance of
needless tests or inappropriate medications. When in doubt about the description, having the client videotape the episode can be very
helpful.