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I have had a few difficulties finding answers for the questions below. I have tried answering the first two myself; but, I am not sure they are correct or not. And I am not too sure about the third one.
In which structure of the brain does the axon from the spinocerebellum tract synapese? Is it the cerebellum?
Are the cell bodies of axon in the gracile tract located at the dorsal root, tectospinal tract located in cerebral cortex?
Which region of spinal cord carries feed-forward information to help accommodate for upcoming motor movement?
Yes, the spinocerebellar tract ends in the ipsilateral cerebellum.
The gracile tract is a bundle of axon fibers in the dorsal root. The neural cell bodies are in the dorsal root ganglions. The tectospinal tract is part of extrapyramidal tract that connects midbrain (mesencephalon) with the spinal cord.
Didin't get exactly what you meant but: the lateral corticospinal tract (part of pyramidal tracts) controls fine movement of ipsilateral limbs, while the anterior corticospinal tract (part of the pyramidal tracts) conducts voluntary motor impulses from the precentral gyrus.
Source: Wikipedia: Tectospinal tract, Spinocerebellar tract, Dorsal root ganglion, Pyramidal tracts, Anterior corticospinal tract, Lateral corticospinal tract.
Neurological examination of the sensory system
Like the motor system, the sensory pathway plays an important role in the transmission and interpretation of environmental stimuli. Without adequate sensory input, appropriate motor responses could not be generated. The two systems work synergistically to provide optimum perception and response to the ever-changing external environment. As a result, it is equally important for clinicians to understand the inner workings of the sensory pathway, how it can be assessed, and what are the signs of sensory dysfunction.
This article will first review the dermatome maps and ascending spinal tracts as a solid understanding of both is creates an invaluable foundation. Subsequently, the article will go on to discuss the examination of the common sensory modalities and what signs are considered abnormal.
|Dermatome||Area of skin supplied by a single nerve|
|Ascending tracts of the spinal cord||Spinothalamic, dorsal column, spinocerebellar, cuneocerebellar, spinotectal, spino-olivary|
|Sensory exam||Introduction & informed consent, adequate exposure, inspect for SWIFT, pain, light touch, temperature, vibration sense, proprioception, graphesthesia & stereognosis, Romberg's test|
|SWIFT||Scars, wasting, involuntary movements, fasciculations, tremors|
Development of spinal neurons and tracts in the zebrafish embryo
We have analyzed pathfinding by growth cones in the spinal cord of the early zebrafish embryo, because it is an extremely simple system. At 18–20 hours of development the spinal cord contains approximately 18 lateral and presumably post-mitotic cell bodies per hemisegment. Of these 8–11 have projected growth cones by 18 hr of development and fall into five classes of neurons (Bernhardt et al., J. Comp. Neurol, preceding paper), including a set of mechanosensory (RB) neurons, three classes of interneurons (DoLA, ascending commissural, and VeLD), and previously characterized primary motor neurons (Eisen et al., '86: Nature 320:269–271). Of these five classes we analyzed pathfinding by the RB, DoLA, early ascending commissural, and VeLD neurons. These neurons are distinguishable at the earliest stages of axonogenesis based on the location of their somata and the number and initial directionality of their growth cones. In each case they follow stereotyped, cell-specific pathways to reach their termination sites. Up through larval stages exuberant axons have not been observed.
The longitudinal axons of each neuronal class form bundles in the early cord. This apparently occurs because growth cones extend in close association with the longitudinal axons of the same neuronal class. At later stages spatially discrete commissural tracts are found in the cord suggesting that commissural growth cones may follow earlier commissural axons as well.
Overview of the Nervous System
The nervous system has two distinct parts: the central nervous system (the brain and spinal cord) and the peripheral nervous system (the nerves outside the brain and spinal cord).
The basic unit of the nervous system is the nerve cell (neuron). Nerve cells consist of a large cell body and two types of nerve fibers:
Axon: A long, slender nerve fiber that projects from a nerve cell and can send messages as electrical impulses to other nerve cells and muscles
Dendrites: Branches of nerve cells that receive electrical impulses
Normally, nerves transmit impulses electrically in one direction—from the impulse-sending axon of one nerve cell (also called a neuron) to the impulse-receiving dendrites of the next nerve cell. At contact points between nerve cells, (synapses), the axon secretes tiny amounts of chemical messengers (neurotransmitters). Neurotransmitters trigger the receptors on the next nerve cell dendrites to produce a new electrical current. Different types of nerves use different neurotransmitters to convey impulses across the synapses. Some of the impulses stimulate the next nerve cell, whereas others inhibit it.
The brain and spinal cord also contain support cells called glial cells. These cells are different from nerve cells and do not produce electrical impulses. There are several types, including the following:
Astrocytes: These cells provide nutrients to nerve cells and control the chemical composition of fluids around nerve cells, enabling them to thrive. They can regulate the neurotransmitters and the external chemical environment around nerve cells to influence how often nerve cells send impulses and thus regulate how active groups of nerve cells may be.
Ependymal cells: These cells form along open areas in the brain and spinal cord to create and release cerebrospinal fluid, which bathes cells of the nervous system.
Glial progenitor cells: These cells can produce new astrocytes and oligodendrocytes to replace those destroyed by injuries or disorders. Glial progenitor cells are present throughout the brain in adults.
Microglia: These cells help protect the brain against injury and help remove debris from dead cells. These cells can move around in the nervous system and can multiply to protect the brain during an injury.
Oligodendrocytes: These cells form a coating around nerve cell axons and make a specialized membrane called myelin, a fatty substance that insulates nerve axons and speeds the conduction of impulses along nerve fibers.
Schwann cells are also glial cells. However, these cells are in the peripheral nervous system rather than in the brain and spinal cord. These cells are similar to oligodendrocytes and make myelin to insulate axons in the peripheral nervous system.
The brain and spinal cord consist of gray and white matter.
Gray matter consists of nerve cell bodies, dendrites and axons, glial cells, and capillaries (the smallest of the body’s blood vessels).
White matter contains relatively very few neurons and consists mainly of axons that are wrapped with many layers of myelin and of the oligodendrocytes that make the myelin. Myelin is what makes the white matter white. (The myelin coating around the axon speeds the conduction of nerve impulses—see Nerves.)
Nerve cells routinely increase or decrease the number of connections they have with other nerve cells. This process may partly explain how people learn, adapt, and form memories. But the brain and spinal cord rarely produce new nerve cells. An exception is the hippocampus, an area of the brain involved in memory formation.
The nervous system is an extraordinarily complex communication system that can send and receive voluminous amounts of information simultaneously. However, the system is vulnerable to diseases and injuries, as in the following examples:
Oligodendrocytes may become inflamed and lost, causing multiple sclerosis.
Bacteria or viruses can infect the brain or spinal cord, causing encephalitis or meningitis.
A blockage in the blood supply to the brain can cause a stroke.
Injuries or tumors can cause structural damage to the brain or spinal cord.
Neurologic exam & localization
Performing a good neurologic examination with proper neurolocalization is critical for devising a suitable list of differential diagnoses with subsequent treatment plans with patients presenting with neurological diseases. The aim of this post is to review functional neuroanatomy and neurolocalization as it pertains to lesions within the central and peripheral nervous systems.
Aspects of the neurologic examination
As with any examination, being consistent is immensely important. This should begin with reviewing the complete history and performing a full physical examination. The neurologic examination can then be focused upon, again with attention to consistency and documentation.
- Sensorium – mentation general observations and interaction with the environment
- Gait and posture – ambulation, ataxia, paresis/plegia, lameness
- Postural reactions – conscious proprioception, hopping, wheel barrowing, tactile and visual placing
- Muscle tone, size, and segmental reflexes
- Myotatic reflex
- Withdrawal reflexes
- Perineal reflex
- Cutaneus trunci reflex
The key to performing an accurate neurologic examination is perfecting one’s examination skills, first on a normal patient. Once one feels confident in knowing what is “normal”, comfort in identifying the “abnormal” and localizing the lesion will come more naturally.
When trying to gain a neuroanatomical diagnosis, it is always best to start broadly, then narrow the focus. The intent of the neurologic exam is to “interrogate” or evaluate different aspects of the nervous system that are specific to a particular area. Although there will inevitably be some overlap, ideally the multi-faced aspect of the exam will help indicate the location of the lesion.
- Cerebrum and diencephalon (thalamus, hypothalamus, etc.)
- Brainstem and cerebellum
With an anatomic diagnosis, one can determine a reasonable list of differential diagnoses, with significance granted using the previously reviewed evaluation of signalment and history.
- D – degenerative
- A – anomalous
- M – metabolic
- N – neoplasia nutritional
- I – infectious inflammatory idiopathic
- T – traumatic toxicity
- V – vascular
While it is important to have an understanding of neuroanatomy from a global veterinary perspective, being a good clinician does not require an in-depth knowledge of neuroanatomy. Clinical neurology requires only an understanding of functional neuroanatomy and lesion localization is, to a large extent, a matter of pattern recognition. That being said, there are a few neuroanatomical pathways that are important to know (e.g., visual pathway, sympathetic pathway leading to Horner Syndrome, cutaneus trunci reflex).
After performing a complete neurological exam, as well as a general physical exam and orthopedic exam (especially if any lameness or weakness), there are two questions that you should ask yourself:
- Does this patient have neurological disease?
- If yes, where is the likely location of disease (neurolocalization)?
This may seem very simplistic, but they are important questions to ask yourself with every patient. Never assume that a patient that is weak or unable to walk has a herniated disc or other neurological disorder. Many non-neurologic conditions mimic neurologic disease. For example, a dog that has bilateral cranial cruciate ligament tears or a cat with aortic thromboembolism may be unable to walk.
The next step is to consider each of the individual neurologic abnormalities noted on exam and identify where the lesion could be located for each abnormality. This is how I teach students that are first learning how to localize lesions.
Case example: You are presented a cat with a sudden onset of circling to the right. On neurologic exam, you discover an absent menace response in the left eye and postural reaction deficits in the left thoracic and pelvic limbs. Now formulate a list of abnormalities and possible lesion locations.
Look back at your list to see if one lesion location is present in all of the abnormalities. For this patient, the only location listed for all three abnormalities is the right forebrain. Next, ask yourself if this makes sense to you. The patient is circling, which also can be seen with vestibular disease, but did you see any other clinical signs that would suggest vestibular dysfunction (e.g., head tilt, nystagmus, ataxia)? Always try to localize the lesion to one location, but never forget that multifocal disease is possible.
The nervous system can be divided into several functional regions where disease leads to a “typical” group of clinical signs referred to as neurologic syndromes.
- Forebrain (cerebrum, thalamus)
- Vestibular – peripheral or central
- C1-C5 spinal cord
- C6-T2 spinal cord
- T3-L3 spinal cord
- L4-S3 spinal cord
A great deal of day-to-day clinical neurology involves pattern recognition. As you become more experienced with the neurologic exam and neurolocalization, you’ll start to recognize these particular syndromes and be able to localize the lesion without having to mentally or physically formulate a list as described above. Listed below are the common clinical signs associated with each functional region of the nervous system, adapted from the excellent veterinary neurology textbook, Clinical Syndromes in Veterinary Neurology by Kyle G. Braund, 2nd ed.
The forebrain includes all structures rostral to the midbrain, including the cerebral hemispheres, thalamus, hypothalmus, epithalamus, and subthalamus. The thalamus is anatomically the rostral end of the brainstem, but is functionally similar to the cerebrum.
Common clinical signs of forebrain dysfunction
- Behavior change and/or loss of trained habits (e.g., urinating/defecating in house)
- Circling toward side of lesion
- Compulsive pacing or wandering aimlessly
- Head pressing, staring off into space, or getting stuck behind furniture or in tight spaces
- Head turn toward side of lesion
- Contralateral postural reaction deficits
- Contralateral vision deficits
- Mental status changes (dull, stupor, coma) – most often with diffuse forebrain disease due to limbic system dysfunction
- Endocrine signs are possible if hypothalmus or pituitary gland dysfunction
The brainstem consists of the midbrain, pons, and medulla oblongata. Some people separate the clinical signs associated with dysfunction of the midbrain, pons, and medulla oblongata, but it’s often difficult and, quite frankly not very common, to cleanly localize the lesion to just the midbrain or pons. It’s certainly possible for a patient to show only dysfunction of cranial nerves III or IV suggesting midbrain disease, but patients more commonly have clinical signs referable to multiple areas of the brainstem.
Important structures in the brainstem include the nuclei giving rise to most of the cranial nerves (III-XII), the Ascending Reticular Activating System (ARAS) controlling level of consciousness, the chemoreceptor trigger zone, and the heart rate and respiratory centers. Additionally, the primary gait generators for dogs and cats are located in the brainstem (likely midbrain), involving the extrapyramidal tracts (e.g., rubrospinal tract).
The proprioceptive and corticospinal motor tracts cross in the midbrain. As a result, lesions cranial to the midbrain (i.e., prosencephalon) will cause contralateral postural reaction deficits and/or weakness, while lesions caudal to the midbrain (pons, medulla, cerebellum, spinal cord) will cause ipsilateral deficits.
Common clinical signs of brainstem disease
- Altered mental status (dull, stupor, coma, disoriented)
- Weakness and ataxia (tetraparesis, ipsilateral hemiparesis)
- Cranial nerve deficits (III-XII possible)
- Postural reaction deficits (ipsilateral unless lesion is cranial midbrain where they’re contralateral)
- Central vestibular dysfunction
- Irregular respiration
DIstinguishing peripheral from central vestibular dysfunction. NOTE: Disorientation is possible for both PVD and CVD, but patients with PVD should remain responsive. Care should also be taken localizing the lesion in patients whose only sign of central vestibular dysfunction is vertical nystagmus. Some patients with PVD will appear to have a vertical nystagmus when it actually has a slight rotational component.
The vestibular system is responsible for maintaining normal body position and coordination. The vestibular system is divided into two portions, the peripheral vestibular system (inner ears, vestibulocochlear nerve) and the central vestibular system (brainstem). There are also vestibular structures in the cerebellum (fastigial nucleus, flocculus, nodulus) and caudal cerebellar peduncle. Dysfunction in these areas of the cerebellum typically causes paradoxical central vestibular signs (see below).
With classic vestibular dysfunction, the head tilt and vestibular ataxia are usually toward the side of the lesion and the fast phase of nystagmuus is away from the side of the lesion (nystagmus “runs away” from the lesion). Postural reaction deficits are always ipsilateral to the lesion and indicate the patient has central vestibular dysfunction. Be careful during the early stage of severe, acute vestibular dysfunction because the nystagmus will occasionally look vertical, but it’s actually rotary. In addition, postural reaction testing may be difficult in moderately to severely affected patients. Try to give the patient at least 24 hours before definitively calling a patient central vestibular and/or considering euthanasia (unless other clear signs of central disease are present). Many patients with severe vestibular dysfunction will improve and even return to normal. This is definitely a “don’t judge a book by its cover” situation.
Paradoxical central vestibular dysfunction
At times, the abnormalities noted on exam are suggestive of central vestibular disorder (e.g., vertical nystagmus, postural reaction deficits), but the signs do not follow the “rules” listed above. This is called paradoxical central vestibular dysfunction and is due to disease in the cerebellum or caudal cerebellar peduncle. The paradox occurs because the head signs suggest a lesion on one side of the body, while the postural reaction deficits indicate the other side. Believe the postural reaction deficits as they are always ipsilateral to the lesion in patients with vestibular dysfunction. Occasionally, animals with cerebellovestibular dysfunction will have an absent menace response with intact vision (ruling out an optic nerve lesion) and intact palpebral reflex (ruling out a facial nerve lesion). As with postural reaction deficits, absent menace response is always ipsilateral to the lesion in patients with cerebellovestibular dysfunction.
Case example: A 10-year-old MC Greyhound is presented to you with an acute onset of non-progressive clinical signs of right head head tilt, vestibular ataxia, resting & positional left rotary nystagmus, and left-sided postural reaction deficits. In this patient, the head tilt and nystagmus suggest a right-sided lesion while the postural reaction deficits suggest a left-sided lesion. The neuroanatomic diagnosis for this patient would be left paradoxical central vestibular.
Bilateral peripheral vestibular dysfunction
Otitis interna is the most common cause of bilateral peripheral vestibular dysfunction, but bilateral signs certainly can be observed in patients with other conditions (e.g., hypothyroidism). These patients often are presented with signs of vestibular dysfunction, including vestibular ataxia (often to both directions) and horizontal or rotary nystagmus. Many of these patients do not have a head tilt, or they have a head tilt that intermittently changes sides. Patients often walk low to the ground or crouched and will have wide side-to-side lateral head excursions.
Vestibular dysfunction due to thalamic disease
Just to confuse things even more, central vestibular signs occasionally occur secondary to a thalamic lesion, most often due a thalamic infarct. This is not very common. It is more important to remember the basic rules of localizing peripheral vs. central dysfunction.
The cerebellum is responsible for rate and range of motion, fine motor control, and equilibrium.
Common clinical signs of cerebellar dysfunction
- Dysmetria – most often hypermetria (“goose stepping”)
- Truncal ataxia
- Intention tremors
- Vestibular signs
- Ipsilateral postural reaction deficits
- Occasional ipsilateral absent menace response (with normal vision, palpebral and no forebrain signs)
- +/- Anisocoria (pupil dilated contralateral to lesion)
- +/- Opisthotonus
C1-C5 spinal cord
Disease in this region of the spinal cord typically causes signs of UMN dysfunction in all 4 limbs.
Common clinical signs of cervical (C1-5) myelopathy
- Weakness/paralysis and/or ataxia in all 4 limbs (tetraparesis/tetraplegia), ipsilateral limbs (hemiparesis/hemiplegia) or only one thoracic limb (monoparesis/monoplegia)
- UMN signs in all 4 limbs
- Normal to exaggerated spinal nerve reflexes
- Normal withdrawal reflex all 4 limbs
- Normal to increased muscle tone in affected limbs
- Late disuse muscle atrophy
- Cervical vertebral discomfort, muscles spasms, rigidity
- +/- UMN bladder
- +/- Respiratory difficulty (UMN dysfunction to phrenic and intercostal nerves)
- +/- Horner Syndrome (1st order sympathetic neurons)
C6-T2 spinal cord
Disease in this region of the spinal cord typically causes signs of LMN dysfunction in the thoracic limbs and UMN dysfunction in the pelvic limbs. However, patients with C6-T2 disease may have normal thoracic limbs and abnormal pelvic limbs, especially with compressive spinal cord lesions (e.g., intervertebral disk protrusion/herniation). This is because the pelvic limb spinal tracts are more peripherally located than the centrally located lower motor neuron cell bodies in the ventral horn of the grey matter. Mild to moderate external compression of the spinal cord will compress the pelvic limb tracts first causing UMN signs to the pelvic limbs, while still having normal thoracic limbs. As the compression worsens, the thoracic limb LMNs are affected leading to LMN signs in the thoracic limbs as well. Cervical discomfort/rigidity is often present to help distinguish C6-T2 signs from a T3-L3 lesion.
Common clinical signs of cervicothoracic (C6-T2) myelopathy
- Weakness/paralysis or ataxia in all 4 limbs (tetraparesis/tetraplegia), ipsilateral limbs (hemiparesis/hemiplegia) or only one thoracic limb (monoparesis/monoplegia)
- Decreased myotatic & withdrawal reflexes in thoracic limbs
- Normal to exaggerated myotatic & withdrawal reflexes in pelvic limbs
- Postural reaction deficits in thoracic and pelvic limbs
- Early denervation atrophy of thoracic limb(s) and late onset disuse muscle atrophy in pelvic limbs
- +/- Cervical pain, muscle spasms, rigidity
- +/- Root signature
- +/- Decreased or absent cutaneous trunci
- +/- UMN bladder
- +/- Respiratory difficulty (LMN dysfunction to phrenic and UMN to intercostal nerves
- +/- Horner Syndrome (1st order sympathetic neurons)
T3-L3 spinal cord
Disease in this region of the spinal cord typically causes signs of UMN dysfunction in the pelvic limbs and normal thoracic limbs.
Common clinical signs of thoracolumbar (T3-L3) myelopathy
- Spastic weakness/paralysis and ataxia in pelvic limbs
- Normal to exaggerated spinal nerve reflexes in pelvic limbs
- Normal withdrawal reflexes in the pelvic limbs
- Postural reaction deficits in pelvic limbs
- Late onset disuse muscle atrophy
- +/- Decreased or absent cutaneus trunci reflex (usually 1-2 vertebrae cranial to cutoff)
- +/- Paravertebral pain at site of lesion
- +/- UMN bladder
- +/- Schiff-Sherrington posture
TIP: To help decide whether a patient has UMN signs to all 4 limbs (C1-C5) or Schiff-Sherrington posture with a T3-L3 myelopathy, closely evaluate the postural reactions in the thoracic limbs. With support, a patient with Schiff-Sherrington posture will usually have normal postural reactions in the thoracic limbs, while a patient with a C1-C5 lesion will have delayed or absent postural reactions. Obviously, the presence of thoracic or lumbar discomfort would suggest Schiff-Sherrington while cervical discomfort/rigidity would suggest a C1-C5 lesion.
L4-S3 spinal cord
Disease in this region of the spinal cord typically causes signs of LMN dysfunction in the pelvic limbs and normal thoracic limbs.
Common clinical signs of a lumbosacral (L4-S3) myelopathy
- Flaccid weakness/paralysis and ataxia in pelvic limbs
- Decreased to absent spinal nerve & withdrawal reflexes in pelvic limbs
- Postural reaction deficits in pelvic limbs
- Decreased to absent muscle tone in affected limb(s) or tail
- Early denervation muscle atrophy
- +/- Decreased or absent cutaneus trunci reflex (lesion is usually 1-2 vertebrae cranial to cutoff)
- +/- Paravertebral pain at site of lesion
- +/- Root signature
- +/- LMN bladder
- +/- Decreased/absent anal tone or dilated anus
- +/- Urinary or fecal incontinence
The neuromuscular system consists of the peripheral nerves, neuromuscular junction, and muscles.
Common clinical signs of neuromuscular dysfunction
- Flaccid paresis / paralysis
- Reduced/absent spinal nerve reflexes
- Postural reaction deficits
- Decreased muscle tone
- Denervation muscle atrophy
- Decreased/absent spinal nerve & withdrawal reflexes, usually without muscle atrophy
- Postural reaction deficits
- Decreased pain response
- Abnormal sensation/sensitivity (paraesthesia) of face, trunk or limbs
- Autonomic neuropathy (alone or in combo with above)
- Anisocoria or dilated pupils
- Decreased tear production
- Decreased salivation
- Generalized weakness
- Exercise intolerance
- Stiff, stilted gait
- Localized or generalized muscle atrophy
- Generalized muscle hypertrophy
- Dimple contracture
- Painful response to muscle palpation
- Limited joint movement (contracture)
- De Lahunta A, Glass E. Veterinary Neuroanatomy and Clinical Neurology. St. Louis, MO: Saunders 2009.
- King AS. Physiological and Clinical Anatomy of the Domestic Mammals: Central Nervous System. NY, NY: Oxford University Press, 1987.
- Vite CH, Braund KG. Braund’s Clinical Neurology in Small Animals: Localization, Diagnosis, and Treatment. Online http://www.ivis.org/advances/Vite/toc.asp 2006.
About the authors
Dr. Riggs received her undergraduate degree in biochemistry from Smith College before pursuing her veterinary degree at the University of Pennsylvania. After graduating in 2010, Dr. Riggs completed a rotating internship followed by a three-year residency in neurology and neurosurgery at The Animal Medical Center in New York City. Dr. Riggs became board certified in 2015.
Dr. Riggs takes pride in being a conservative surgeon who performs surgery aggressively when indicated. Her primary interests are in diagnostic MRI and finding non-surgical options for complex neurological diseases. Dr. Riggs also enjoys performing advanced neurosurgical procedures.
Dr. Troxel received his veterinary degree from the Iowa State University College of Veterinary Medicine in 1999. Following veterinary school, Dr. Troxel completed a rotating internship in small animal medicine, surgery and critical care at VCA South Shore Animal Hospital in South Weymouth, MA in 2000. He then went on to complete an internal medicine internship at Garden State Veterinary Specialists in New Jersey in 2001. From 2001 to 2004, Dr. Troxel was at the University of Pennsylvania’s School of Veterinary Medicine to complete a residency in medical neurology and neurosurgery. Dr. Troxel became board-certified in neurology by the American College of Veterinary Internal Medicine in July 2004. He has also received a neurosurgery certificate of training. Following his residency, Dr. Troxel served as the staff neurologist at VCA South Shore Animal Hospital until he joined the Neurology/Neurosurgery Department at Massachusetts Veterinary Referral Hospital in 2005.
In addition to his love of neurology and neurosurgery, Dr. Troxel is also interested in the use of technology to better care for patients and their owners and to improve efficiency in the veterinary clinic.
Ramsay Hunt syndrome associated with spinal trigeminal nucleus and tract involvement on MRI
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J. Ramsay Hunt established the term herpes zoster oticus in 1907. This syndrome is caused by the reactivation of latent varicella-zoster virus (VZV) residing within the geniculate ganglion with subsequent spread of the inflammatory process to the seventh and eighth cranial nerves. Features may include ipsilateral facial paralysis, tinnitus, hearing loss, hyperacusis, vertigo, dysgeusia, decreased tearing, and ear pain. Characteristic vesicles are frequently seen in the external auditory canal, on the pinna, and less often on the anterior pillar of the fauces. In some patients, cranial nerves V, IX, and X are also involved. MRI often demonstrates segmental enhancement of the seventh and eighth cranial nerves, geniculate ganglion, and parts of the membranous labyrinth. 1 We report a patient with Ramsay Hunt syndrome (RHS) in whom MRIs showed a T2-weighted hyperintense lesion involving the ipsilateral spinal trigeminal nucleus and tract (STNT).
The spinal cord extends caudally from the medulla at the foramen magnum and terminates at the upper lumbar vertebrae, usually between L1 and L2, where it forms the conus medullaris. In the lumbosacral region, nerve roots from lower cord segments descend within the spinal column in a nearly vertical sheaf, forming the cauda equina.
The white matter at the cord’s periphery contains ascending and descending tracts of myelinated sensory and motor nerve fibers. The central H-shaped gray matter is composed of cell bodies and nonmyelinated fibers (see figure Spinal nerve). The anterior (ventral) horns of the “H” contain lower motor neurons, which receive impulses from the motor cortex via the descending corticospinal tracts and, at the local level, from internuncial neurons and afferent fibers from muscle spindles. The axons of the lower motor neurons are the efferent fibers of the spinal nerves. The posterior (dorsal) horns contain sensory fibers that originate in cell bodies in the dorsal root ganglia. The gray matter also contains many internuncial neurons that carry motor, sensory, or reflex impulses from dorsal to ventral nerve roots, from one side of the cord to the other, or from one level of the cord to another.
The spinothalamic tract transmits pain and temperature sensation contralaterally in the spinal cord most other tracts transmit information ipsilaterally. The cord is divided into functional segments (levels) corresponding approximately to the attachments of the 31 pairs of spinal nerve roots.
Degenerative Spine Conditions
This page provides an overview of spinal anatomy, a quick glossary, a description of symptoms that prompt evaluation by a neurosurgeon, and an explanation of common tests and treatments for degenerative spine conditions.
The Spine Hospital at The Neurological Institute of New York is recognized around the world as a leader in the treatment of degenerative spine conditions.
Degenerative spine conditions all involve a loss of normal structure and function in the spine. Degenerative means that the cause of these changes is age-related wear and tear. The changes are not due to trauma, infection, or some other cause.
To understand degenerative spine conditions, it helps to understand a little about basic spinal anatomy.
The spine is composed of many vertebrae , or individual bones of the spine, stacked one on top of another. Together, this stack forms the vertebral column . The topmost section of the vertebral column, the section in the neck, is called the cervical spine. The next section, located in the upper and mid-back, is called the thoracic spine. (The vertebrae of the thoracic spine articulate with, or form joints with, the ribs.) Below the thoracic spine is the lumbar spine, in the lower back. Finally, the sacral spine is located below the small of the back, between the hips. Sturdy intervertebral discs connect the vertebrae. The intervertebral discs act as cushions and shock absorbers between the vertebrae. Each disc is composed of a jelly-like core surrounded by a fibrous outer ring.
In the cervical, thoracic, and lumbar spine, all vertebrae are essentially similar. Each vertebra (the singular of vertebrae) is composed of two sections. One, the vertebral body , is a solid, cylindrical segment, shaped something like a marshmallow. It provides strength and stability to the spine. The other segment is an arch-shaped section of bone called the vertebral arch . Projecting from the back of the vertebral arch are segments of bones, called processes , that articulate with each other and provide attachment points for muscles, ligaments and tendons. The vertebral arch is connected to the vertebral body by two small columns of bone called the pedicles . Together, the vertebral body, the pedicles, and the vertebral arch form a ring of bone around a hollow center. Stacked on top of one another in the spinal column, these rings align to form a long, well-protected channel known as the spinal canal .
Inside the well-protected spinal canal is the spinal cord , the delicate bundle of nerves and other tissue that connects brain and body. The spinal canal also houses the beginning of the spinal nerve roots . These are the nerves that leave the spine, exiting the spinal canal through foramina (small openings) to branch out to the body. The spinal cord and nerve roots are suspended in a liquid called the cerebrospinal fluid . Membranes called the meninges act somewhat like the casing on a sausage, wrapping up the spinal cord, the nerve roots, and the CSF inside the spinal canal. The outermost layer of the meninges is a tough tissue layer known as the dura mater .
Degenerative spinal changes can affect almost every structure of the spine. For example:
- Discs: Intervertebral discs usually change with age. They lose some of their ability to cushion the joints, and their fibrous outer portions may crack, allowing some of the jelly-like core to protrude. This condition is called a herniated disc. They may also slightly collapse and dry out, a condition called degenerative disc disease.
- Bones and cartilage: As cartilage at the joints wears down, the vertebrae or the bony processes at the back of the vertebral arch may rub against one another. This stimulates the growth of bone spurs (extra bone) that may restrict the joints’ range of motion, may cause stiffness and pain, and may compress the nerve roots and spinal cord.
- Ligaments: Ligaments may thicken, causing stiffness and pain or compressing nerve roots or the spinal cord.
- Compression: To neurosurgeons, compression means harmful pressure on the spinal cord or nerve roots. Bone spurs, thickened ligaments, and herniated discs are all possible sources of compression. (Each of these conditions can also exist without causing compression.)
- Myelopathy: A reduction in the spinal cord’s ability to send signals between brain and body. Causes weakness, numbness, clumsiness, and/or bowel and bladder incontinence. Can be caused by compression of the spinal cord .
- Radiculopathy: A reduction in a nerve root’s ability to send signals between spinal cord and body. Causes pain, weakness, or numbness in the area served by that nerve root–for example, the arms or the backs of the legs. Can be caused by compression of a nerve root .
- Stenosis: a narrowing of the spinal canal. Stenosis can compress the spinal cord or nerve roots and may lead to myelopathy or neurogenic claudication.
- Arthritis: joint inflammation that causes pain and stiffness. The most common type is osteoarthritis , which occurs when cartilage in the joints wears down.
- Bone spurs: extra bone that may grow on joints affected by osteoarthritis. Bone spurs may compress the spinal cord or nerve roots.
- Nonsurgical treatments: Treatments such as physical therapy, medication, heat and cold, etc. Nonsurgical treatments avoid the risks of surgery, and are the best choice for certain cases of degenerative conditions. Arthritis and disc herniation, for example, are best treated nonsurgically when they do not cause spinal cord or nerve root compression. (Also called nonoperative treatments.)
- Surgical treatments: Surgical treatment is necessary to treat compression that causes myelopathy and certain cases of radiculopathy. While there are many specific procedures that remove pressure from the spinal cord and nerve roots, they may be grouped under the general heading of decompressive surgery .
Degenerative spine conditions vary widely in their presentation. Some cause no symptoms at all. When symptoms do occur, they often include back pain or neck pain. Other symptoms depend on the location and type of problem.
Many degenerative conditions do not require surgical treatment, but some may. “Red flags” for evaluation by a neurosurgeon include:
- Back pain accompanied by bowel or bladder incontinence and/or numbness in the areas that would sit on a saddle (so-called saddle anesthesia )—may indicate cauda equina syndrome, a rare neurological condition that should be treated promptly
- Neck or back pain that includes weakness, numbness, or pins-and-needles in the arms or legs–may indicate myelopathy
- Neck or back pain that radiates (spreads) into the shoulder, arm, hand, leg, or foot–may indicate radiculopathy
- Neck or back pain accompanied by fever
- Neck or back pain that gets worse during the night
- Neck or back pain accompanied by unexplained weight loss
- Neck or back pain that continues for several weeks or months
- Neck pain accompanied by difficulty breathing or swallowing
- Neck or back pain following a fall, injury or other trauma
Tests and Diagnosis
If a patient presents with symptoms associated with degenerative spine disorders, the doctor may order the following tests:
- X-ray (also known as plain films) –test that uses invisible electromagnetic energy beams (X-rays) to produce images of bones. Soft tissue structures such as the spinal cord, spinal nerves, the disc and ligaments are usually not seen on X-rays, nor are most tumors, vascular malformations, or cysts. X-rays provide an overall assessment of the bone anatomy as well as the curvature and alignment of the vertebral column. Spinal dislocation or slippage (also known as spondylolisthesis), kyphosis, scoliosis, as well as local and overall spine balance can be assessed with X-rays. Specific bony abnormalities such as bone spurs, disc space narrowing, vertebral body fracture, collapse or erosion can also be identified on plain film X-rays. Dynamic, or flexion/extension X-rays (X-rays that show the spine in motion) may be obtained to see if there is any abnormal or excessive movement or instability in the spine at the affected levels.
- Magnetic resonance (MR) imaging – provides a detailed image of soft tissue like discs, nerves and the spinal cord. This scan allows the doctor to see how the nerves and spinal canal space are affected by degenerative spine conditions.
- Computed tomography (CT) scan – provides a detailed image of bone structures in the spine. A CT scan uses computers and X-rays, and provides much more detail than a plain X-ray.
- Myelography / post myelogram CT – provides images that can help determine whether bulging or herniated discs are compressing the spinal cord or nerve roots. Performed by injecting a contrast dye into the spinal column and taking several X-rays and, usually, a CT scan.
- Electromyography (EMG) – tests the electrical activity of a nerve root to help determine the cause of pain.
- Discogram – helps determine whether pain is due to a damaged intervertebral disc. Performed by injecting a contrast dye into the disc and taking several X-rays while also asking the patient about symptoms.
Since the causes of degenerative spine conditions will vary from patient to patient, no two treatments will be identical.
Before surgery is considered, nonoperative treatments may be recommended. These measures include:
- Medications (pain medications, anti-inflammatory medications, antidepressants, anticonvulsants, non-steroidal anti-inflammatory drugs (NSAIDs), topical opioids, and/or epidural injections of steroids or pain medication)
- Activity modification
- Patient education on proper body mechanics (to help decrease the chance of worsening pain or damage to the disc)
- Physical therapy (will focus on strengthening the muscles of the back/neck and improving flexibility as well as range of motion)
- Weight control
In some cases, surgery may be recommended or required to treat a degenerative condition. The type of procedure depends on the type of condition and its severity. Surgery is considered when:
- A patient’s symptoms do not respond to nonoperative measures
- A patient’s pain is severe
- Myelopathy is present
In such cases, surgery has the potential to relieve pain, prevent further damage to the spinal cord, and drastically improve a patient’s quality of life. Procedures include:
- Anterior cervical discectomy with fusion (ACDF)
- Anterior cervical corpectomy with fusion
- Laminectomy to remove bone spurs or a section of the lamina (part of the vertebral arch) to make room for the spinal cord
- Laminoplasty to remove part of the lamina to make room for the spinal cord
In some situations, the surgeon may also need to perform a spinal fusion to ensure the spinal column is stable. During a spinal fusion, the surgeon will place a bone graft between the vertebrae to cause the bones to fuse (grow together).
For a detailed explanation of specific degenerative spine conditions, refer to the individual pages.
Preparing For Your Appointment
Drs. Paul C. McCormick, Peter D. Angevine and Dr. Patrick C. Reid are experts in treating degenerative spine conditions. They can also offer you a second opinion.
- Department of Neurosurgery, Pt. B.D. Sharma University of Health Sciences, Rohtak, Haryana, India
- Department of Radiodiagnosis, Pt. B.D. Sharma University of Health Sciences, Rohtak, Haryana, India
- Department of Anaesthesiology and Critical Care, Pt. B.D. Sharma University of Health Sciences, Rohtak, Haryana, India
Department of Neurosurgery, Pt. B.D. Sharma University of Health Sciences, Rohtak, Haryana, India
Copyright: © 2015 Singh I. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Singh I, Rohilla S, Kumar P, Sharma S. Spinal dorsal dermal sinus tract: An experience of 21 cases. Surg Neurol Int 07-Oct-20156:
How to cite this URL: Singh I, Rohilla S, Kumar P, Sharma S. Spinal dorsal dermal sinus tract: An experience of 21 cases. Surg Neurol Int 07-Oct-20156:. Available from: http://surgicalneurologyint.com/surgicalint_articles/spinal-dorsal-dermal-sinus-tract-an-experience-of-21-cases/
Date of Submission
Date of Acceptance
Date of Web Publication
Background:Spinal dorsal dermal sinus is a rare entity, which usually comes to clinical attention by cutaneous abnormalities, neurologic deficit, and/or infection. The present study was undertaken to know the clinical profile of these patients, to study associated anomalies and to assess the results of surgical intervention.
Methods:Medical records of 21 patients treated for spinal dorsal dermal sinus from September 2007 to December 2013 were reviewed.
Results:We had 21 patients with male: female ratio of 13:8. Only 2 patients were below 1-year of age, and most cases (15) were between 2 and 15 years (mean age = 8.2 years). Lumbar region (11 cases) was most frequently involved, followed by thoracic (4 cases), lumbosacral, and cervical region in 3 patients each. All of our patients presented with neurological deficits. Three patients were admitted with acute meningitis with acute onset paraplegia and had intraspinal abscess. The motor, sensory, and autonomic deficits were seen in 14, 6, and 8 patients, respectively. Scoliosis and congenital talipes equinovarus were the common associated anomalies. All patients underwent surgical exploration and repair of dysraphic state and excision of the sinus. Overall, 20 patients improved or neurological status stabilized and only 1 patient deteriorated. Postoperative wound infection was seen in 2 cases.
Conclusions:All patients with spinal dorsal dermal sinuses should be offered aggressive surgical treatment in the form of total excision of sinus tract and correction of spinal malformation, as soon as diagnosed.
Keywords: Complication, dermal sinus, dysraphism, presentation, spine
There are different types of neurogenic bladder depending on the underlying cause. Many of these types may have similar symptoms.
Uninhibited bladder is usually due to damage to the brain from a stroke or brain tumor. This can cause reduced sensation of bladder fullness, low capacity bladder and urinary incontinence. Unlike other forms of neurogenic bladder, it does not lead to high bladder pressures that can cause kidney damage. 
In spastic neurogenic bladder (also known as upper motor neuron or hyper-reflexive bladder), the muscle of the bladder (detrusor) and urethral sphincter do not work together and are usually tightly contracted at the same time. This phenomenon is also called detrusor external sphincter dyssynergia (DESD). This leads to urinary retention with high pressures in the bladder that can damage the kidneys. The bladder volume is usually smaller than normal due to increased muscle tone in the bladder. Spastic neurogenic bladder is usually caused by damage to the spinal cord above the level of the 10th thoracic vertebrae (T10).  
In flaccid bladder (also known as lower motor neuron or hypotonic bladder), the muscles of the bladder lose ability to contract normally. This can cause the inability to void urine even if the bladder is full and cause a large bladder capacity. The internal urinary sphincter can contract normally, however urinary incontinence is common. This type of neurogenic bladder is caused by damage to the peripheral nerves that travel from the spinal cord to the bladder. 
Mixed type of neurogenic bladder can cause a combination of the above presentations. In mixed type A, the bladder muscle is flaccid but the sphincter is overactive. This creates a large, low pressure bladder and inability to void, but does not carry as much risk for kidney damage as a spastic bladder. Mixed type B is characterized by a flaccid external sphincter and a spastic bladder causing problems with incontinence. 
Neurogenic bladder can cause a range of urinary symptoms including urinary urgency, urinary incontinence or difficulty urinating (urinary retention.) The first sign of bladder dysfunction may be recurrent urinary tract infections (UTIs). [ citation needed ]
Neurogenic bladder can cause hydronephrosis (swelling of a kidney due to a build-up of urine), recurrent urinary tract infections, and recurrent kidney stones which may compromise kidney function.  This is especially significant in spastic neurogenic bladder that leads to high bladder pressures. Kidney failure was previously a leading cause of mortality in patients with spinal cord injury but is now dramatically less common due to improvements in bladder management. 
Urine storage and elimination (urination) requires coordination between the bladder emptying muscle (detrusor) and the external sphincter of the bladder. This coordination can be disrupted by damage or diseases of the central nervous system, peripheral nerves or autonomic nervous system.  This includes any condition that impairs bladder signaling at any point along the path from the urination center in the brain, spinal cord, peripheral nerves and the bladder.
Central nervous system Edit
Damage to the brain or spinal cord is the most common cause of neurogenic bladder. Damage to the brain can be caused by stroke, brain tumors, multiple sclerosis, Parkinson's disease or other neurodegenerative conditions.  Bladder involvement is more likely if the damage is in the area of the pons. Damage to the spinal cord can be caused by traumatic injury, demyelinating disease, syringomyelia, cauda equina syndrome, or spina bifida. Spinal cord compression from herniated disks, tumor, or spinal stenosis can also result in neurogenic bladder.  
Peripheral nervous system Edit
Damage to the nerves that travel from the spinal cord to the bladder (peripheral nerves) can cause neurogenic bladder, usually the flaccid type. Nerve damage can be caused by diabetes, alcoholism, and vitamin B12 deficiency. Peripheral nerves can also be damaged as a complication of major surgery of the pelvis, such as for removal of tumors. 
The diagnosis of neurogenic bladder is made based on a complete history and physical examination and may require imaging and specialized studies. History should include information on the onset, duration, triggers, severity, other medical conditions and medications (including anticholinergics, calcium channel blockers, diuretics, sedatives, alpha-adrenergic agonist, alpha 1 antagonists).   Urinary symptoms may include frequency, urgency, incontinence or recurrent urinary tract infections (UTIs). Questionnaires can be helpful in quantifying symptom burden.  In children it is important to obtain a prenatal and developmental history. 
Ultrasound imaging can give information on the shape of the bladder, post-void residual volume, and evidence of kidney damage such as kidney size, thickness or ureteral dilation. A voiding cystourethrography study uses contrast dye to obtain images of the bladder both when it is full and after urination which can show changes in bladder shape consistent with neurogenic bladder. 
Urodynamic studies are an important component of the evaluation for neurogenic bladder. Urodynamics refers to the measurement of the pressure-volume relationship in the bladder. The bladder usually stores urine at low pressure and urination can be completed without a dramatic pressure rise. Damage to the kidneys is probable if the pressure rises above 40 cm of water during filling.  Bladder pressure can be measured by cystometry, during which the bladder is artificially filled with a catheter and bladder pressures and detrusor activity are monitored. Patterns of involuntary detrusor activity as well as bladder flexibility, or compliance, can be evaluated. The most valuable test to test for detrusor sphincter dyssynergia (DESD) is to perform cystometry simultaneously with external sphincter electromyography (EMG).  Uroflowmetry is a less-invasive study that can measure urine flow rate and use it to estimate detrusor strength and sphincter resistance.   Urethral pressure monitoring is another less-invasive approach to assessing detrusor sphincter dyssynergia.  These studies can be repeated at regular intervals, especially if symptoms worsen or to measure response to therapies. 
Evaluation of kidney function through blood tests such as serum creatinine should be obtained. 
Imaging of the pelvis with CT scan or magnetic resonance imaging may be necessary, especially if there is concern for an obstruction such as a tumor. The inside of the bladder can be visualized by cystoscopy.
Treatment depends on the type of neurogenic bladder and other medical problems. Treatment strategies include catheterization, medications, surgeries or other procedures. The goals of treatment is to keep bladder pressures in a safe range and eliminate residual urine in the bladder after urination (post-void residual volumes). [ citation needed ]
Emptying the bladder with the use of a catheter is the most common strategy for managing urinary retention from neurogenic bladder. For most patients, this can be accomplished with intermittent catherization which involves no surgery or permanently attached appliances. Intermittent catheterization involves using straight catheters (which are usually disposable or single-use products) several times a day to empty the bladder.  This can be done independently or with assistance. For people who are unable to use disposable straight catheters, a Foley catheter allows continuous drainage of urine into a sterile drainage bag that is worn by the patient, but such catheters are associated with higher rates of complications. 
Oxybutynin is a common anti-cholinergic medication used to reduce bladder contractions by blocking M3 muscarinic receptors in the detrusor.  Its use is limited by side effects such as dry mouth, constipation and decreased sweating. Tolterodine is a longer acting anticholinergic that may have fewer side effects. 
For urinary retention, cholinergics (muscarinic agonists) like bethanechol can improve the squeezing ability of the bladder. Alpha blockers can also reduce outlet resistance and allow complete emptying if there is adequate bladder muscle function. 
Botulinum Toxin Edit
Botulinum toxin (Botox) can be used through two different approaches. For spastic neurogenic bladder, the bladder muscle (detrusor) can be injected which will cause it to be flaccid for 6–9 months. This prevents high bladder pressures and intermittent catherization must be used during this time. 
Botox can also be injected into the external sphincter to paralyze a spastic sphincter in patients with detrusor sphincter dyssynergia. 
There are various strategies to alter the interaction between the nerves and muscles of the bladder, including nonsurgical therapies (transurethral electrical bladder stimulation), minimally invasive procedures (sacral neuromodulation pacemaker), and operative (reconfiguration of sacral nerve root anatomy). 
Surgical interventions may be pursued if medical approaches have been maximized. Surgical options depend on the type of dysfunction observed on urodynamic testing, and may include:
- Creation of a stoma (from the intestines, called "conduit") that bypasses the urethra to empty the bladder directly through a skin opening. Several techniques may be used. One technique is the Mitrofanoff stoma, where the appendixor a portion of the ileum (‘Yang-Monti’ conduit) are used to create the diversion.  The ileum and ascending colon can also be used to create a pouch accessible for catheterization (Indiana pouch). or urethral sphincterotomy are other surgical approaches that can reduce bladder pressures but require use of an external urinary collection device.  may be used in both adults and children  have shown good term outcomes in adults and pediatric patients.  One study on 97 patients followed for a mean duration of 4 years found that 92% percent were continent at day and night during follow up.  However, patients in this study who had intermediate-type bladders underwent adjuvant cystoplasty.
- Bladder Neck Closure is a major surgical procedure which can be a last resort treatment for incontinence, a Mitrofanoff stoma is necessary to empty the bladder. 
The overall prevalence of neurogenic bladder is limited due to the broad range of conditions that can lead to urinary dysfunction. Neurogenic bladder is common with spinal cord injury and multiple sclerosis.  Rates of some type of urinary dysfunction surpass 80% one year after spinal cord injury.  Among patients with multiple sclerosis, 20–25% will develop neurogenic bladder although the type and severity bladder dysfunction is variable. 
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