Neurology Basics

Comes from greek a-taxis: without order or without coordination

Incoordination during voluntray movement without paresis, spasticity or involuntary movement

Ataxia is usually associated with a wide base stance and incoordination of the limbs

Cerebellar ataxia = abnormal rate, range, or force of movement with intact strength

Vestibular ataxia = loss of balance; animal often lists or falls to one side

Proprioceptive ataxia = decreased awareness of limb position and often results in scuffing of toes, crossing oflimbs, and standing on the dorsum of paws

1. Abnormal proprioception (sensory ataxia)-any Dz causing compression of SC or otherwise affecting proprioceptive tracts in SC or brain

CSx: absent or reduced knuckling respons, postural responses (ie hopping reaction) may also be abnormal. May see additional signs of Sc dysfunction (paresis etc)

2. Cerebellar dysfucntion: may arise from many Dz's (congenital malformation, infection, abiotrophy)

CSx: typically assoc with symmetric ataxia, dysmetria (eg goose stepping gait), intention tremors (esp of head)

3. Vestibular Dz: common in dogs and cats and may be idiopathic, associated with middle/inner ear Dz or associated with brain stem Dz

CSx: asymmetric ataxia, head tilt, nystagmus and falling or rolling to one side

Paresis is the partial loss of voluntary motor actvity (ie reduced ability to initiate motor activity)

Paraylsis or plegia is the complete loss of voluntary motor activity

Depression: Lethargy with decreased activity but normal mental status

Obtundation: Dull mentation with decreased consciousness and response to mild stimulus

Stupor: Decreased consciousness and response only to noxious stimulus

Coma: Unconscious and no response to even noxious stimulus

The RAS in the rostral midbrain controls the level of consciousness, and any Dz process affecting this area of uts connections to the cerebral cortex will alter consciousness

Coma or stupor results from one of three Dz processes:

1. Encephalopathy (metabolic or toxic)

2. Diffuse cerebral cortical Dz

3. Dz in the midbrain or pons (compression, destructive lesions)

Most important aetio: increased ICP, cerebral oedema, herniation of brain tissue

From Latin proprius, meaning "one's own", "individual," (think of "to appropriate an object"; ad + proprius-->to make ones own) and capio, capere, to take or grasp, is the sense of the relative position of neighbouring parts of the body and strength of effort being employed in movement

Means "sense of position"

Clinical sign of loss of proprioception is ataxia (in coordination)

Increase in muscle tone due to hyperexcitable stretch (myotactic) reflexes

Descending UMN pathways normally attenuate the myotactic reflex. Lesions in the UMN pathway cause changes in the excitability of motor neurons, interneuronal connections and local reflex pathways that over time lead to hyperexcitable myotactic reflexes and spasticity

Sustained muscle contraction that is worsened by stimulation

It occurs with: strychnine poisoning, some congenital conditions

Rhythmic oscillation of the body or body part due to alternating contractions of antagonistic muscles

Can be: intention tremor, resting tremor, fine fast action tremor or static tremor

No signs of altered mental status or proprioceptive positioning deficits

No positional nystagmus (nystagmus is always in the same direction) and is either horizontal or rotatory NOT vertical

Head tilt towards affected side

Ipsilateral ataxia

Fast phase of nystagmus AWAY from affected side

Changes in mental status (most commonly somnolence) and deficits in proprioceptive positioning and/or hopping

Nonambulatory tetraparesis common

vertical or positional nystagmus may be seen

Characterized by dysmetria (inability to control the rate and range of stepping movements) which is usually manifested as hypermetria (exaggerated step-hyperflexion)

Diff from spasticity: spasticity causes thoracic limbs to appear rigid or spastic while hypermetria is manifested by prolonged flexion of the step (protraction)

Other signs: truncal sway, head/whole body tremors, intentional tremors, wide pelvic limb stance and gait

Other signs: coexisting vestibular (possible), mentation WNL, tone/reflexes generally WNL (sever signs->increased tone), proprioception normal to delayed (ipsi)

Septic:

Non septic

Idiopathic:

Intracranial

Extracranial

1. Gait normal or abnormal?

Normal:

2. Postural reactions:

Deficits-->Cerebrum/diencephalon

Normal-->neuropathy of cranial nerves

Abnormal Gait:

2. Type of gait abnormality

Tetraparesis/hemiparesis

*UMN signs-->Brainstem

*LMN signs-->generalized LMN disorder

Asymmetric ataxia, head tilt, proprioception normal, direction of nystagmus doe snot change, facial paresis, Horner's syndrome

-->Peripheral vestibular Dz

For these puposes functional brainstem; midbrain, pons, medulla oblongata

UMN signs in all four limbs (tetraparesis) or hemiparesis (depends on site)

Paresis/paralysis caused by brainstem dysfunction is obvious in gait and postural reactions

good for cf with forebrain elsions-->minimal gait abnormalities (have postural deficits/walking or circling)

CN signs (III-XII) with larger or extensive brainstem lesions. Help localize lesion

Mental status may be altered (esp if there are lesions in midbrain or pons)-dullness to coma

CN dysfunction will be ipsilateral to lesions

Motor dysfunction (ie gait) can be contraletral or ipsilateral depdning on pathways affected

May produce UMN signs in all 4 limbs (tetraparesis) or hemiparesis

Gait is not severly afafcted but postural deficits may be seen

May circle in eitehr direction depending on lesion

CN II may be affected-visual and PLR deficits

SOL of dinecephalon may also affect CN III, IV and VI

CN signs are ipislateral to lesion

Postural dfeicits are ontarletarl to lesions or ipislateral to lesion

Characteristic abnormality-->hypothalamic problem

May have generalized hyperesthesia (rare) due to thalamic central role in sensory pathway projection to the cerebral cortex

Altered level of consciousness (stupor or coma) due to interference with ARAS

May be central (brainstem-affecting the nuclei, cerebllum (vestibulocerebellum), sinal cord (vestibulospinal tracts)) or peripheral (affecting the nerve or labyrinth->old dog vestibular Dz)

CANNOT rule out central vestib Dz on neuro exam, can only RULE IN (eg vertical nystagmus, paradoxical head tilt, extra-vestibular signs assoc with brainstem)

Any sign of of brainstem Dz in assoc with vestibular signs indicate that central involvment is present. Most important differentiating feature->deficit in postural reactions

Peripheral vestibular dysfunctio does not cause paresis or loss of proprioception whereas central Dz freq does

May be unilateral or bilateral

Spastic ataxia, wide-based stance, dysmetria, intention tremor, no obvious signs of weakness

Cerebellar ataxia is often characetrized by dysmetria (stride lengths that are too short-hypometria, stride lengths that are too long-hypermetria)

Nystagmus may occur-usually more of a tremor of the globe than the slow-quick movemnts assoc with evstibular Dz

Is most pronounced when animal shifts its gaze and focuses on annew field (intention tremor)

ACute injury to cerebllum can cause decerebellate posture: extensor hypertonus in TL and flexion in PL

Lesions to floculonodular node causes vestibular signs

Diffuse cerebellar lesion-->loss of menace response

Alteration in behaviour or mental status

Seziures

Loss of vision with intact PLR

Contarletral decrease in facial sensation

Mild contarleteral hemiparesis

Deficits in postural reactions

Only one or two of these signs may be present

Signs are generally contraletarl to lesion

Behavioural changes-->often lesion in limbic system/frontal/temporal lobes

Frontal lobe lesion-->disinhibition-->excessive pacing

Pacing will often continue until a barrier is reached and head pressing will occur

If there is an asymmetric lesion ciricling may occur (ipsilateral to lesion) and head TURN (not tilt) towards side of lesion may be seen

Dullness, stupor or coma

Mentation abnormalities usually more severe with brainstem injuries

1. Telencephalon

2. Diencephalon

3. Brainstem (mesencephalon, pons, myelencephalon)

4. Vestibular system

5. Cerebellar

Extensor rigidity of all limbs; secondary to severe cortical/midbrain lesion; patient usuallycomatose

Extensor rigidity of the thoracic limbs with flexion of pelvic limbs and dorsal extension ofthe head; associated with acute cerebellar lesions including herniation

Hyperesthesia: increased sensitivity to sensory stimulus

Anaesthesia: absent response to sensory stimulus

Hypalgesia: decreased sensitivity to painAnalgesia: absent pain perception

GAIT->UMN/GP Ataxia

-slow strided gait

-prolonged swing phase to gait ("floating" end to swing phase)

-knuckling/scuffing

-crossing limbs

Mentation, CN WNL

+/- pain at site of lesion

Proprioception->normal to reduced

Tone->decreased (LMN), normal to increased (UMN)

Reflexes->decreased (LMN), normal to increased (UMN)

Peripheral vestibular Dz

Dogs->most commonly eriatric, GSD

Cats->any age

DDx: peripheral-neoplasia, otitis media/interna, ototoxicity central-malformation, inflamm/infctn, neoplasia, CVA

Investigate well, then provide supportive care (fluids if not drinking, anti emetic to counter motions sickness, keep in hospital to avoid self harm)

If there is gradual or complete improvement within 72 hours, it is likely idiopathic vestibular disease and additional diagnostic testing is not necessary. If there is no improvement or progression of signs, it is likely something much more serious

Gait: normal gait with postural reaction deficits (contralateral to lesion)

NO ataxia, NO weakness

Propulsive gait (constantly pacing, aimless), circling (towards lesion)

Postoral reactions->normal to delayed

Other signs: CN often abnormal, contralateral visual deficit with NORMAL PLR, contrlateral facial hypalgesia, facial/tongue paralysis, ALTERED MENTATION, ALTERED BEHAVIOUR (lack of recognition of environ, may be more aggressive or more docile, propulsive, SEZIURES)