Where is the lesion questions

The nervous system is divided into the central nervous system CNS and peripheral nervous system. The central nervous system is comprised of the brain and spinal cord. Cranial and spinal nerves make up the peripheral nervous system. The brain consists of two cerebral hemispheres, the brain stem, and the cerebellum.

The cerebral cortex is a convoluted structure with multiple tortuous folds called gyri separated by deep grooves called sulci. The central sulcus separates the frontal lobe from the parietal lobe, and the Sylvian fissure marks the upper boundary of the temporal lobe.

An arbitrary line separates the occipital lobe from the parietal and temporal lobes. The precentral gyrus serves as the primary motor cortex and is the command and control center for voluntary movements. Pyramidal cells in the layer V of the cerebral cortex innervate lower motor neurons located in the cranial and spinal motor nuclei through corticobulbar and corticospinal tracts, respectively.

These pyramidal cells are called upper motor neurons. The distribution of these pyramidal cells follows a unique topographic pattern. Upper motor neurons that control lower motor neurons of the lower limb are located on the medial side, and those innervating lower motor neurons of the upper limb are located laterally. An area on the lateral surface of the dominant frontal lobe, the left frontal lobe in most individuals, is the motor control center for speech. Another area at the junction of parietal and temporal lobes analyzes sensory input related to speech and is called Wernicke's area.

The brain stem consists of the midbrain, pons, and medulla. Some cranial nerves leave the brain stem. Descending fibers of the corticospinal tract travel from the cerebral cortex to corona radiata, posterior limb of the internal capsule, cerebral peduncles, pons, and medulla. At the lower part of the medulla, most of these fibers cross the midline, continue as the lateral corticospinal tract and descend through the white matter of the cord to innervate the anterior horn cells. This crossing over of corticospinal tract fibers is called pyramidal decussation.

Resultantly, pyramidal cells of the right cerebral cortex innervate left spinal motor nuclei and vice versa. Spinal motor nuclei innervating skeletal muscles of upper and lower limbs receive upper motor neuron innervation only from the contralateral side. Lower motor neurons of cranial nerves, on the other hand, are innervated by corticobulbar fibers from both sides.

Therefore despite damage to corticobulbar fibers on one side, cranial motor nuclei will continue to receive upper motor supply from the other side. The nucleus of the facial nerve, however, can be considered a hybrid. Like other cranial motor nuclei, the upper half of the facial nucleus receives bilateral upper motor neuron innervation. On the other hand, the lower half receives innervation only from the contralateral side. Medulla oblongata passes through the foramen magnum and continues as the spinal cord.

The spinal cord has multiple segments. Each segment gives away a pair of spinal nerves. There are 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 2 coccygeal segments. Looking at the cross-section, the spinal cord has a central gray matter that contains cell bodies of spinal nuclei and peripheral white matter that contains myelinated axons.

Tetraparesis or tetraplegia with decerebrate rigidity, conscious proprioception deficits and intact spinal reflexes are often seen with brain stem disease. Ipsilateral cranial nerve deficits are possible in isolation or in conjunction with central motor and sensory dysfunction, depending on whether the cranial nerve is affected after it has exited the brainstem or before respectively.

In addition to the above signs, there is the potential for cardiac and respiratory abnormalities, including apnoea and cardiac arrest. The function of the vestibular system is to send messages to the brain about the gravitational forces acting on the head and any movement that the head experiences.

The brain can then determine the position of the head in space and can coordinate subsequent movements of the eyes and limbs. The peripheral component of the vestibular system is located in the inner ear and is made up of a membranous labyrinth and the vestibular portion of cranial nerve VIII.

This system is intricately associated with the auditory system and is enclosed in the petrous temporal bone close to cranial nerve VII and the sympathetic supply to the eye and face. The central component of the vestibular system consists of vestibular nuclei in the caudal brainstem medulla oblongata and the flocculonodular lobe of the cerebellum.

These nuclei are connected to the nuclei of cranial nerves III, IV, and VI to control the movement of the eyes so that the eyes move in a coordinated fashion with the head.

The vestibular nuclei are also connected via the vestibulospinal tract to the extensor muscles of the neck and the limbs; they are responsible for extensor tone in the ipsilateral limbs and cause contralateral extensor inhibition.

Damage to either the peripheral or the central components of the vestibular system will cause vestibular dysfunction. It is most common to see unilateral lesions and therefore asymmetric signs but bilateral lesions are possible.

The signs exhibited by the patient depend upon the portion of the vestibular system affected. Indeed, it is important to use these differences in lesion localization, as peripheral and central vestibular diseases have several different differentials to be considered as well as different prognoses.

The head tilt is towards the side of the lesion in peripheral disease whereas it can be to any side if there is a central lesion.

Often, there is no head tilt if there is bilateral disease and instead there are wide excursions of the head and neck from side to side. This can progress to rolling, leaning or falling to one side with unilateral lesions. Peripheral vestibular disease occurs without any deficits in conscious proprioception or strength, whereas a central lesion may cause these abnormalities.

The direction of the nystagmus is often described as the direction of the fast phase but can be horizontal, rotational or vertical in its direction. In normal animals, a physiologic nystagmus should be induced by rotation of the head, with the direction being in the plane of the head movement and the fast phase being towards the side of rotation this may also be termed the occulocephalic reflex.

This may be altered or absent in animals with vestibular disease. Nystagmus can be spontaneous which means that it occurs when the head is stationary in a normal position.

With unilateral peripheral lesions, the fast phase is away from the side of the disease and the direction can be horizontal or rotational. With central lesions, the fast phase is usually away from the side of the disease but the direction can be vertical as well as horizontal or rotatory. If the nystagmus is detected only when the head is placed in an unusual position, this is called positional nystagmus and can occur with both peripheral and central lesions but may be more common with the latter.

Animals with bilateral disease usually do not have spontaneous or positional nystagmus. The ventrally deviated eye is usually on the side of the lesion.

Occasionally, a constant ventral strabismus is present with vestibular disease. It is possible that multiple cranial nerve defects be present with central vestibular disease. Cerebellar disease is one of the most readily recognizable syndromes in veterinary practice.

The cerebellum coordinates movements. It controls the rate and range of movements but not the initiation of the movement itself. Cerebellar disease results in an inability to regulate the rate, range, and force of a movement i.

Clinical signs include an exaggerated limb response when a movement is initiated, such as "goose-stepping" hypermetria when walking. Limb movements are typically spastic and clumsy. Initiation of movement is delayed and often accompanied by tremors i. Tremors are especially noticeable involving the head. Intention tremors disappear at rest. Fine, pendular, or oscillatory eye movements also may be present. A bilateral menace deficit may be noted, although vision is not affected.

If the lesion involves only one side of the cerebellum, the menace deficit will be ipsilateral. The delirium, mydriasis, hypertension, dry mouth, urinary retention, and constipation of atropine overdose reflect blockade of muscarinic cholinergic receptors. Often, it is best to start from the periphery and work centrally, considering each of the possible sites listed in the table below.

The middle column lists the terms commonly used to describe the disease processes affecting these areas and the right column lists the symptoms and signs typical of lesions at these sites.

This is where your knowledge of neuroanatomical pathways and the signs and symptoms that go along with damage to these pathways comes in. Since the nervous system is a continuum, a particular symptom may represent a lesion at multiple levels. Thus, a complaint of weakness may represent dysfunction at the level of the muscle, neuromuscular junction, peripheral nerve, plexus, spinal nerve root, lateral column of the spinal cord, pyramidal tract in the brainstem, internal capsule, or cerebral motor cortex.

It is thepatternof weakness e. So, for example, weakness, numbness, and reflex loss within the distribution of a particular spinal nerve root implies a radiculopathy, whereas weakness of the face, arm, and leg all on the same side of the body implies a lesion within the motor pathways above the level of the facial nucleus in the mid-pons.

A patient with monocular blindnessmust havea lesion on the same side somewhere between the cornea and optic chiasm. A patient with an absent tendon reflexmust havea lesion within the afferent-efferent arc serving that reflex. If the lesion is here, does it explainallthe findings? If the answer is no, you should carefully re-examine the data and your conclusions. Either the localization is wrong or the disease process is multi-focal or diffuse.

If the lesion is here, whatelseshould be present? With this small amount of information face and unilateral , we can already narrow down the possible sites of involvement to peripheral nerve cranial nerve VII within subarachnoid space or temporal bone, brainstem pontine lesion affecting the VII nerve nucleus or fascicles , or supranuclear motor pathways supplying the face e.

But we obviously need to do better than this before beginning to address what the patient has. The first question should be what is the pattern of weakness?

If the patient has lower facial weakness drooping at the corner of the mouth or inability to raise the corner of the mouth when smiling with relative sparing of the upper face, this is consistent with an upper motor neuron lesion a. If instead the patient has weakness that involves the entire half of the face equally facial droop as well as inability to close the eye , this is consistent with a lower motor neuron lesion at the level of the VII nerve or the VII nerve nucleus in the pons.

Our patient complains of both facial droop and inability to close the eye. So now we need to differentiate between a pontine lesion and a peripheral nerve lesion.

What neighborhood signs would you expect with a lesion of the facial nucleus or intrapontine nerve fibers? The parapontine reticular formation lies just ventromedial to the abducens nucleus.

So an associated ipsilateral lateral rectus palsy or conjugate gaze palsy would localize the lesion to the pons. Since the facial nerve fibers pass between bundles of corticospinal tract fibers, an associated contralateral hemiparesis would also localize the lesion to the pons. What if instead of associated diplopia or contralateral arm and leg weakness, the patient complains of hearing loss and tinnitus? This suggests involvement of the auditory nerve.

The two places that the facial nerve is in close proximity to the auditory nerve are within the cerebellopontine angle Figure 2 and within the temporal bone. If we wanted to, we could localize a VII nerve lesion even more precisely in terms of where the lesion is in relation to the departure of the nerve to the stapedius muscle, the chorda tympani, and the greater superficial petrosal nerve based on the presence or absence of hypersensitivity to sound, loss of taste, and impaired lacrimation, respectively.

Why bother doing this? It is not a simple exercise in mental masturbation; rather it is an exercise that allows us to begin to address etiology. The pathophysiological processes underlying an intrinsic pontine lesion e.

A neoplasm, an infarct, and demyelination in the right frontal lobe will all cause left-sided weakness, but at different rates time-intensity profile and with different individual features headache, seizures, papilledema, episodic waxing and waning, aggravation by heat, etc. You need to know what the very first symptom was.

Patients often pick the most dramatic events and play down earlier subtle details. Ask for earlier, perhaps less obvious symptoms of the same thing. Warning signs. It must have been something I ate. This piece of history is crucial. You must dig for it.