Should your patient choose to visit an ANIC neurologist for evaluation & imaging within 2 weeks of your ANIC Tele-Neurology consultation, the tele-neurology fee will be deducted from the appointment fee.
For recheck examinations, complete as much of the following neurology form as appropriate. You may leave questions/sections blank and simply proceed to the next question/section if not relevant.
Please upload any video footage pertinent to the case. Please include any specific inquiries or comments about the videos in the space provided below each video window. You can limit your teleneurology consult to include only video footage and related comments or proceed to The ANICs neurological exam form and include as much information as you have available.
for a Menace Response tutorial, click here
for a Pupillary Light Reflex tutorial, click here.
for a Palpebral Reflexes & Nasal Sensation tutorial, click here.
for Nystagmus tutorial, click here
for a Gait Assessment tutorial, click here.
for a Hopping tutorial, click here.
for a Placing tutorial, click here.
for a Patellar Reflexes tutorial, click here.
for a Withdrawal / Flexor Reflexes tutorial, click here.
for a Cutaneous Trunci Reflex tutorial, click here.
for a Perineal Reflex tutorial, click here.
for a Muscle Tone tutorial, click here
For a Nociception (Pain Sensation) tutorial, click here.
The prosencephalon/forebrain is the area of the brain located rostral to the tentorium cerebelli (supratentorial region). It includes the cerebral cortex and white matter, basal nuclei, diencephalon (divided in thalamus, subthalamus, metathalamus and hypothalamus). The cerebral cortex is important for behavior, vision, hearing, fine motor activity and conscious perception of touch, pain (nociception), temperature and body position (conscious proprioception). The cerebral white matter mainly conveys ascending and descending sensory and motor activities. The basal nuclei are involved in muscle tone, initiation and control of voluntary motor activity. The diencephalon is the most rostral part of the brainstem. It is responsible for control of autonomic (appetite, thirst, temperature, electrolyte and water balance) and endocrine functions, sleep and consciousness. It also is involved in olfactory function (CN I: olfactory nerve projects to the hypothalamus and other parts of the limbic system), vision and pupillary light reflex (CN II: optic nerve and optic chiasm are located on the ventral surface of the hypothalamus) and acts as a visual (lateral geniculate nucleus), nociceptive and proprioceptive sensory relay system to the cerebral cortex. Finally, the cell bodies of upper motor neurons are located in the motor cortex (pyramidal system), the diencephalon and motor centre of the brainstem (extrapyramidal system).
The brainstem is ventral to the two cerebral hemispheres and the cerebellum. A neuroanatomic diagnosis of “brainstem” is used to denote lesions that include the midbrain, pons, and medulla oblongata. Functionally, the brainstem contains the paired cranial nerve nuclei, the regulatory centers for consciousness (ARAS) and respiration, and descending motor and ascending sensory pathways. Thus, cranial nerve abnormalities, behavioral changes, loss of key autonomic functions, and a loss of strength and coordination may be present with brainstem disease. [NB: Although anatomically the diencephalon (primarily comprised of the thalamus) is the rostral extent of the brainstem, it is considered part of the forebrain / prosencephalon in lesion localization.]
The brainstem connects the cerebral hemispheres to the spinal cord via ascending sensory (GP) and descending motor pathways (UMNs). Similar to C1-C5 spinal cord lesions, UMN tetraparesis (through tetraplegia) and general proprioceptive (GP) deficits may accompany brainstem disease. Because of the presence of vestibular nuclei in the pons and medulla, vestibular ataxia may be present and superimposed upon GP ataxia.
Depending on the region of the mid to caudal brainstem affected, dysfunction of the cranial nerves III-XII may be present. The neurologic examination allows for assessment of the diverse motor and sensory functions of the cranial nerves. Lesions affecting the cranial nerves in the caudal brainstem typically cause ipsilateral postural reaction deficits because of their impact on the UMN and GP systems. The presence of cranial nerve abnormalities and normal postural reactions suggests a peripheral (cranial) neuropathy; however, an early or slowly compressive brainstem lesion cannot be excluded. If there is ambiguity in postural reaction testing, a neurodiagnostic workup should be considered.
Neurologic Signs That May Be Associated with Mid to Caudal Brainstem Disease:
UMN tetraparesis (or tetraplegia) and GP deficits; vestibular ataxia (pontine or medullary lesions); opisthotonus (midbrain lesions)
Ipsilateral deficits (pons and medulla), contralateral deficits (rostral midbrain)
Normal to increased (all four limbs)
Hypalgesia of trunk and limbs may be present (rare)
Anisocoria (III, sympathetics); dropped jaw (V bilateral); atrophy of muscles of mastication (V); facial hypalgesia (V); head tilt (VIII); resting or positional nystagmus (VIII); abnormal physiologic nystagmus (III, IV, VI, VIII); resting or positional strabismus (III, IV, VI, VIII); facial paresis or paralysis (VII); dysphagia (IX, X); tongue paresis or paralysis (XII)
Respiratory or cardiac abnormalities
GP, General proprioceptive; UMN, upper motor neuron.
The spinal cord is composed of a central core of grey matter containing cell bodies of sensory, interneuron and lower motor neurons. The cell bodies of efferent neurons are present in the ventral (somatic motor neuron responsible for innervation of striated muscles) and lateral grey column (cell bodies of preganglionic sympathetic neurons in the thoracic segments and preganglionic parasympathetic neurons in the sacral segments). The cell bodies of afferent (sensory) neurons are present in the dorsal root ganglion. The outer portion of the spinal cord is composed of white matter divided in three columns or funiculi. The dorsal funiculus consists essentially of ascending tracts mainly involved in proprioception. The lateral funiculus contains both ascending (proprioception, touch, pressure, temperature and pain pathways) and descending (motor pathways) tracts. The ventral funiculus contains only descending motor tracts.
A spinal cord segment is defined as a portion of the spinal cord, which gives rise to one pair of spinal nerves. There are eight cervical, thirteen thoracic, seven lumbar, three sacral and at least two caudal spinal cord segments. Some spinal cord segments lie in the vertebra of the same annotation while others do not. Neurological lesion localisation refers to spinal cord segments. Innervation in the body is organized in a segmental pattern. Each cutaneous region of the body (dermatome) and group of muscle fibers (myotome) is innervated by one or more spinal cord segment. Functionally, the spinal cord can be divided in four regions: cranial cervical [C1 to C5] – cervico-thoracic [C6 to T2] – thoraco-lumbar [T3 to L3] and lumbo-sacral [L4 to S3]. LMN cell bodies are located within the grey matter of the cervico-thoracic intumescence (segments [C6 to T2]) for the thoracic limbs and lumbo-sacral intumescence (segments [L4 to S3]) for the pelvic limbs. Lesions at the level of the intumescences result in LMN signs in the corresponding limb(s).
The vestibular system is the primary sense that governs balance. Just as vision depends on the eyes to convert light to electrical impulses and then requires a specialized region of the brain to interpret the information correctly, the vestibular system also depends on two components. These are the inner ear structures that convert information about head position into electrical impulses and then an area of the brainstem that interprets this information.
An animal can have a disturbance of balance due to either a problem affecting the inner ear, such as a severe and deep-seated ear infection or tumor. Alternatively, the problem could be located in the vestibular center of the brainstem caused by a stroke, a brain tumor, autoimmune inflammation or an infection.
The signs of vestibular disease include not only a loss of balance but also commonly a head tilt and nystagmus. Nystagmus is an involuntary eye movement where the eyes flicker repetitiously, with a rapid a slow phase. Sometimes other nerves of the head become dysfunctional with vestibular disease such as the facial nerve, which is required for normal blinking and tear production.
The diagnosis depends first on a full neurological examination to differentiate inner ear problems (aka “peripheral vestibular disease”) from brainstem disorders (aka “central vestibular disease”). Depending on the examination results, the structures of the ear and brainstem may need to be imaged using either a CT scan or an MRI. In addition, a sample of spinal fluid may need to be evaluated. Treatment and prognosis will depend on the results of these tests. The prognosis is generally good for peripheral vestibular disease but is more guarded for central vestibular disease. Complications are dependent on the specific diagnosis.
The LMN unit consists of the nerve cell body in the ventral gray matter of the CNS, ventral nerve root, peripheral nerve, and muscle. Disease of any component of this unit will produce LMN signs. Normal strength depends not only on functional LMN unit, but also on effective neuromuscular transmission via acetylcholine (Ach) across the neuromuscular junction (NMJ). Diseases affecting neuromuscular transmission (e.g., myasthenia gravis, tick paralysis), so-called junctionopathies, may produce LMN signs that are indistinguishable from neuropathies and myopathies.
Because NMDs may mimic one another, the neurologic examination rarely confirms the exact component of the LMN unit that is affected. The clinician may require ancillary tests (CK, AST, Tensilon testing, acetylcholine receptor antibody titer, electrodiagnostics, nerve and muscle biopsies) to further localize the problem to the nerve, muscle, or NMJ. The LMN unit may be affected diffusely or individual peripheral or cranial nerves may be affected. When cranial nerve deficits (e.g., facial paresis) are present, these must be interpreted with other neurologic findings in order to differentiate neuromuscular disease from a brainstem disorder.
Neuromuscular weakness is characterized by flaccidity and depressed or absent spinal reflexes. Postural reactions typically are normal with pure NMDs (no sensory nerve involvement), although the patient must be well supported or may fail postural testing on account of weakness. Ambulatory patients with pure NMDs typically have a “short and choppy” gait without ataxia because GP. Exercise intolerance may be the only abnormality present in some patients with NMDs.
In some NMDs (e.g., polyneuropathies), involvement of the recurrent laryngeal nerve may lead to a change in, or loss of, voice (dysphonia) and increased inspiratory noise (stridor). The development of megaesophagus in various NMDs may cause regurgitation, often with accompanying aspiration pneumonia. The NMDs also carry the risk of hypoventilation due to involvement of the respiratory muscles. Finally, changes in muscle mass may vary from severe neurogenic atrophy (e.g., brachial plexus avulsion) to “pseudohypertrophy,” which accompanies myopathies (e.g., muscular dystrophy).
Neurologic Abnormalities Associated with LMN/Neuromuscular Dysfunction
Variable: flaccid paresis in affected limb(s) through flaccid paralysis of affected limb(s); exercise may exacerbate the paresis
Delayed to absent in affected limb(s); normal in “pure” LMN disease if patient maintains some voluntary motor function
Decreased tone of affected limb(s); neurogenic atrophy may be severe; pseudohypertrophy in certain myopathies; possible LMN bladder
Variable: hyporeflexia thru areflexia of affected limb(s); possibly reduced perineal reflexes (S1-S3)
Normal in “pure” LMN disease (but if a polyneuropathy with a sensory component, hypalgesia may be present)
Variable: multiple cranial nerves may be affected
Laryngeal paralysis, dysphagia, megaesophagus common with LMN disease
LMN, Lower motor neuron.