Neuro (SACCM / Dobratz / seminal papers) Flashcards
States of consciousness
- Normal
- Obtunded - state of decreased responsiveness / alertness, can be classified as mild, moderate or severe
- Stupor / semicoma - patient only responds to vigorous or painful stimuli
- Coma - patient does not respond to any stimuli. Spinal reflexes might be normal or exaggerated (in absence of other lesions), and CN can be present (depending on the location of the injury)
Abnormalities in mentation indicates lesions where?
Cerebrum or ascending reticular activating system (ARAS) in the brain stem
- Ascending Reticular Activating System - AKA Reticular formation - a network of nuclei in the brainstem that function to activate the cerebral cortex and maintain consciousness.
List metabolic causes of abnormal mentation (at least 10)
Hypoxia Ischemia Kernicterus (hyperbilirrubinemia) Endocrine diseases (hypothyroidism, HHS, Cushing's) Hepatic encephalopathy (liver failure) Uremic encephalopathy (renal failure) Hypoglycemia Electrolyte abnormalities (sodium / water, calcium, magnesium) AB disturbances (acidosis / alkalosis) Pain Sepsis Hypo/hypethermia CNS diseases (seizures, post ictal, meningitis / encephalitis)
5 variables to assess in a patient with decreased mentation
Level of consciousness Motor activity Respiratory pattern Pupil size & responsiveness Oculocephalic reflex
How will our patient be if he has a lesion at or caudal to the midbrain?
Decreased consciousness
Gait abnormalities - ataxia, paresis, plegia
Deficits ipsilateral to the lesion
How will our patient be if the lesion is rostral to the midbrain?
Decreased mentation
Barely any gait abnormalities
No CP reactions on contralateral side
Decerebrate rigidity
Extensor rigidity all 4 limbs
Opisthotonus
Stupor / coma
Lesion on midbrain and/or rostral pons
Decerebellate rigidity
Extension rigidity in front limbs
Extension or flexion on hind limbs depending on where lesion is
Opisthotonus
Normal mentation and voluntary movements
Associated with acute cerebellar injury
Respiratory patterns associated with intracranial disease
- Cheyenne-Stokes - alternating hyperventilation with apnea periods. Diffuse cerebral or thalamus lesions and metabolic encephalopathies.
- Central neurogenic hyperventilation - persistent hyperventilation that can lead to respiratory alkalosis. Midbrain lesions.
- Apneusis - breathing pauses during inspiration - pontine lesion.
- Irregular / ataxic breathing: irregular depth and frequency of breathing, normally leading to permanent apnea. Lower pons or medulla.
Why is important to assess pupil size and reactivity in patients with abnormal mentation?
Pupil size is the result of balance between sympathetic and parasympathetic.
Parasympathetic is important as it is mediated through CN III that goes through midbrain - loss of PS innervation results in mydriasis).
Pupillary abnormalities and lesion localization - unilateral mydriatic unresponsive pupil?
Loss of parasympathetic innervation to the eye. Compression or destruction of the ipsilateral midbrain or CN III - often associated with increased ICP and unilateral cerebral herniation. R/O atropine / tropicamide
Pupillary abnormalities and lesion localization - bilateral miosis?
Metabolic encephalopathies
Diffuse midbrain compression with increased ICP - sometimes precedes bilateral, unresponsive mydriasis
Pupillary abnormalities and lesion localization - bilateral mydriatic unresponsive pupils?
Fixed and dilated pupils.
Severe bilateral compression or destruction of midbrain / CN III, typically from bilateral cerebral herniation - grave prognosis
Drugs that can cause mydriasis / miosis?
Bilateral miosis: opioids, benzodiazepines
Mydriasis: topical atropine, tropicamide
Why it is important to assess the occulocephalic reflex (Dolls eye)?
Physiologic nystagmus or Doll´s eye is a combination of eye movements in response to vestibular input (turning head side to side).
Loss of occulocephalic reflex - lesion on midbrain and pons (medial longitudinal fasciculus) that coordinates CN III, IV and VI
Poor prognosis
What characteristics should have an ideal coma scale?
a. Reliable (measures what it is supposed to measure)
b. Valid (yields the same results with repeated testing)
c. Linear (gives all components equal weight)
d. Easy to use
What does involve the compensation for increased brain tissue volume?
Shifting CSF out of the skull
Decreased CSF production
Eventually, decreased cerebral blood flow.
When are these compensatory mechanisms (for increased brain tissue volume) more effective?
When the increases in ICP are slow
What happens when the capacity for compensation is exhausted?
A further small increase in intracranial VOLUME results in dramatic elevations of IC PRESSURE, with an immediate onset of clinical signs.
See PV curve
How is TBI graded in human medicine and based on what?
a. Mild, moderate or severe
b. Glasgow Coma Scale
What is the modified GCS?
a. A modification of the GCS used in humans, proposed for Veterinary Medicine.
b. Enables grading of the initial neurologic status and serial monitoring of the patient.
c. An almost linear correlation between mGCS and the short-term survival of dogs with head trauma has been evaluated.
What are the categories assessed on the mGCS?
a. Level of consciousness, motor activity (gait and spinal reflexes) and brainstem reflexes (PLR and occulocephalic reflex).
b. Each of these 3 categories are assigned a score from 1 to 6 (lower worst)
Can the motor activity be affected by the level of consciousness?
Yes
What do we need to determine before extensive manipulation of the patient?
Whether spinal cord injury or severe orthopedic abnormalities are present.
How are the spinal reflexes normally in a patient with cerebral injury?
a. They are normal or often exaggerated, and present in all four limbs.
b. Severely affected comatose animals frequently lose muscle tone and reflex activity.
What indicates pupils that respond appropriately to light, even if miotic?
Adequate function of the rostral brainstem, optic chiasm, optic nerves and retinas.
If there is no ocular lesion, what can miosis indicate?
Lesion in the diencephalon, particularly in the hypothalamus as it is the origin of the sympathetic pathway
How can we assess the oculovestibular reflex?
a. With irrigation of the external auditory canal with ice-cold water
b. Absence of eye movements upon this irrigation of cold water is indicative of profound brainstem failure and is an accepted criterion of brain death in humans.
Do we have scales to assess long-term prognosis in veterinary medicine? And in humans?
a. No
b. Yes, the Glasgow Outcome Scale (GOS)
- Why cannot we apply the GOS to veterinary patients?
Because it is based on the ability of the patient to communicate and be self-sufficient.
What is another coma scale that has been introduced in human medicine?
a. FOUR score – Full Outline of UnResponsiveness
b. Includes much more important information than the GCS – measurement of brainstem reflexes, determination of eye opening, blinking and tracking; the presence of abnormal breath rhythms and a respiratory drive.
Do seizures occur more commonly in dogs or in cats?
Dogs
Define seizure
A clinical manifestation of a paroxysmal cerebral disorder, caused by a synchronous and excessive electrical neuronal discharge, originating from the cerebral cortex.
Define cluster seizures
Two or more seizures within a 24h period
Define epilepsy
Recurrent seizures of any type resulting from an intracranial cause.
What is status epilepticus (SE)?
Continuous seizures, or two or more discrete seizures between which there is incomplete recovery of consciousness, lasting at least 5 minutes.
How can we classify seizures?
a. Partial or generalized
b. Partial seizures originate from a focus in one cerebral hemisphere and usually manifest localized clinical sings. Usually have an acquired cause.
c. Generalized seizures are the most commonly recognized seizures in dogs and cats, the most common type is the tonic-clonic seizure.
How can we subclassify partial seizures?
a. Simple or complex partial seizures.
b. Simple partial seizures: there is no alteration in consciousness, and the clinical signs during the seizure are limited to isolated muscle groups (e.g., tonus or clonus of a limb). Additional clinical sings (e.g. autonomic signs) may be present during a simple partial seizure.
c. Complex partial seizures are accompanied by an alteration in consciousness. There might be involuntary or compulsive actions such as chewing, licking and defensive or aggressive behavior. They are AKA as psychomotor seizures.
d. Both types of partial seizures may spread throughout the brain, causing generalized seizures.
What is kindling?
The process by repeated stimulation of the cerebral cortex by a subconvulsive electrical stimulus causes generalized seizures.
What is a mirror focus?
When abnormal electrical activity may be recorded over the contralateral cerebral cortex following establishment of a focal seizure focus.
Why does SE happen?
Because there is a failure of the normal brain homeostasis mechanisms that work to stop seizures => persistent neuronal excitation, inadequate neuronal inhibition or both.
How long can it take for SE to cause brain injury?
a. About 45min – that is in experimental animals – most likely occurs in clinical patients after a much shorter time.
b. SE might cause neuronal necrosis, particularly in brain regions with high metabolic rates.
What is the pathophysiology of SE?
a. In early SE, an increase in blood flow may be protective for the brain
b. In late SE, cerebral blood flow decreases simultaneously as blood pressure decreases and cerebral metabolic rate (e.g. glucose and oxygen use) increases. This leads to ATP depletion and lactate accumulation which contribute to neuronal necrosis.
c. SE may be associated with systemic problems, including hypoxemia, hyperthermia, aspiration pneumonia, systemic lactic acidosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, neurogenic pulmonary edema and AKI.
How can we classify the etiology of seizures?
a. Intracranial vs extracranial
b. Intracranial: progressive vs non-progressive
c. Extracranial: outside the body (toxins) and inside the body (e.g. liver disease) causes.
Mention some causes of progressive intracranial disease
a. Inflammation (GME), neoplasia, nutritional alterations (thiamine deficiency), infection, anomalous entities (hydrocephalus) and trauma.
b. Most animals with progressive IC disease are clinically abnormal between seizures and usually have progression of clinical signs.
Nonprogressive causes of seizures
Inherited epilepsy, infectious, trauma.
What do we need to have as a part of a good diagnostic plan for seizures?
History (important to ask specific seizure history – age at onset, frequency and description of seizures, behavior between seizures and temporal associations), signalment, PE, neurological examination, blood work +/- imaging (CT/MRI), EEG
When is EEG particularly useful?
In patients undergoing treatment for status epilepticus because the external manifestations of seizures may be abolished by drugs.
Does CSF helps provide a definitive diagnosis?
Most of the times is supportive of the diagnosis, however, occasionally provides diagnostic information with some infections (e.g. Cryptococcus neoformans) and some neoplasms (e.g. lymphoma)
What are the goals of anticonvulsant therapy?
Reduce the severity, frequency and duration of seizures to a level that it is acceptable to the owner, without intolerable or unacceptable adverse effects on the animal.
What is the base for a good treatment plan?
a. Treat the underlying disease
b. Select the appropriate anticonvulsant drug
What should be the treatment for SE?
a. Immediate emergency evaluation and treatment (airways, breathing, cardiovascular function, body temperature, glucose concentration and blood pressure)
b. Pharmacologic treatment
c. Mannitol should be considered as cerebral edema occurs often in patients that present in SE.
What are the first line drugs for treatment of SE in dogs and cats?
Diazepam and midazolam
Which drugs are commonly used as maintenance anticonvulsant?
Phenobarbital and levetiracetam.
Why can propofol be used to control seizures?
a. Because it is a rapid-acting, lipid-soluble general anesthetic agent.
b. It is a third line drug for the management of SE in dogs and cats.
c. The anticonvulsant effect is likely because of its GABA agonist activity.
d. Its use is controversial because seizures are associated with its use in humans.
Successful maintenance anticonvulsant therapy depends on what?
On maintenance of plasma concentrations of appropriate anticonvulsant drugs within a therapeutic range defined for the species in which the drug is to be administered.
What are the first line of anticonvulsant drugs recommended for chronic seizure disorders in dogs? And in cats?
a. Phenobarbital and bromide
b. Phenobarbital.
What are the stages of spinal cord injury following trauma?
a. Initial primary tissue damage from direct mechanical disruption
b. Secondary damage via biochemical and vascular events
c. When cellular membrane integrity is disrupted, a complex cascade of biochemical reactions is initiated, including the release of excitotoxic amino acids, free fatty acids, oxygen free radicals and vasoactive agents.
d. NDMA receptors are activated and voltage-sensitive calcium and sodium channels open. These membrane changes result in increased intracellular calcium and sodium, decreased intracellular potassium and increased extracellular potassium.
e. In addition to changes in ionic concentrations, a decrease in blood flow occurs as a result of direct, mechanical compression and/or loss of autoregulation, vasospasm, and hemorrhage, leading to spinal cord ischemia.
f. Ischemia results in cytotoxic edema, axonal degeneration, demyelination, abnormal impulse transmission, conduction block and cellular death.
What signs can be seen with central vestibular disease?
Proprioceptive deficits (ipsilateral), hemiparesis, tetraparesis, altered mental state, dysfunction of other cranial nerves, decerebellate posturing (tis can be intermittent!!!)
