Welcome to the clinical neurology podcast, where you will learn over 12 episodes, how to localise a lesion in neurology based on history taking and physical examination. The podcast is meant for medical students and to make them enjoy learning neurology. Medicine, paediatrics, psychiatry, critical care, neurology residents, general practitioners and nurse practitioners will find it beneficial. Notes, images and other clinical resources for the podcast are available in the show description and on the neurology teaching club.com website. I am your host Dr Krishnadas N C, and let’s get started.
In the last episode we learnt how to approach a case of weakness. We learned that the first step is to make sure that there is true weakness. Once you are sure that there is true weakness the next step is to see if its upper motor neuron or lower motor neuron type of weakness based on bulk, tone, distribution of weakness, reflex, and presence or absence of fasciculation.
Hemiplegia or weakness of one side of the body is a functional deficit which is unless otherwise proved upper motor neuron type. This is because for hemiplegia the lesion is in the pyramidal tract above C5 level which is Upper motor neuron. The lower motor neuron disease is unlikely to affect one side of body alone. Why should Muscle, neuromuscular junction, root, nerve involve one side only? Lower motor neuron disorders like motor neuron disease can rarely produce asymmetrical weakness mimicking hemiplegia but they are rare. For all practical purpose a hemiplegia may be considered as an upper motor neuron problem. This makes hemiplegia a very straight forward case for undergraduate exams and is often kept for the same. Its very important for medical students to have a good idea regarding the localization of hemiplegia.
As already mentioned, the lesion in hemiplegia is in pyramidal tract above C5. The terms pyramidal tract, corticospinal tract and upper motor neuron are often used interchangeably but there is some difference between them. The neurons from which the corticospinal tract and corticobulbar tract arise is called the upper motor neuron. The pyramidal tract name comes from fibers that travel through medullary pyramids which mostly contain corticospinal tract. Strictly speaking corticobulbar fibers which are upper motor neuron fibers to motor cranial nerve nuclei will not be included when we use the terms pyramidal fibers and corticospinal tract. However, a better term is not there for the voluntary descending motor pathway so all three are often used interchangeably. Its important to know the anatomy of corticospinal and corticobulbar tract very well to localize hemiplegia.
The purposive movements are initiated and performed by corticospinal tract. It primarily integrates fine discrete skilled distal movements. It was initially thought that the pyramidal fibres are formed by axons of giant pyramidal cells of Betz in lamina V of primary motor cortex. But only 3% of fibres arise from Betz cells. These are large heavily myelinated axons that conduct rapidly. Only 30% of fibres in CST is formed from primary motor cortex ie the area 4 of pre central gyrus. The rest of the fibres arise from supplementary motor cortex, premotor cortex and also from the post central sensory cortex. The primary motor cortex is connected with opposite motor cortex, supplementary motor cortex, premotor cortex and post central sensory cortex. The supplementary motor cortex is associated with preparation and planning of movement which is executed by primary motor cortex.
The primary motor cortex receives fibres from cerebellum through the posterior division of ventrolateral nucleus of thalamus. The cerebellum plays an important role in fine tuning of movements through this pathway with the help of information regarding JPS it receives from limbs through spinocerebellar pathway. It acts like a conductor of orchestra by modulating the contraction of agonists and antagonists so that the movements have grace and there is no ataxia though it is not directly involved in motor pathway. The basal ganglia also modulate the motor pathway through the thalamocortical connection. We will discuss these in detail when we discuss cerebellum and extrapyramidal system.
Motor homunculus represents the localization of function within the primary motor cortex. Corticospinal system is phylogenetically new and it is only fully evolved in human beings and apes. The phylogenetic development of speech and complex hand function results in larger area for tongue, mouth, lips, thumb and fingers in the motor homunculus. The leg area in motor homunculus extends into the medial surface of frontal lobe where it forms part of anterior part of paracentral lobule which has important role in bowel and bladder function. The medial surface of brain containing the leg area of motor homunculus is supplied by anterior cerebral artery while the lateral surface is supplied by middle cerebral artery. This has clinical localization significance.
The corticospinal tracts are excitatory and mostly use glutamate as neurotransmitter. It ascents in corona radiata to reach the anterior 2/3 of posterior limb of internal capsule. In the internal capsule the fibres to upper extremity is arranged more anteriorly close to corticobulbar fibres which travel in the genu of internal capsule. The corticospinal fibres then ascends down in the middle 3/5 of cerebral peduncle in midbrain, basis pontis and the medullary pyramids. At the lower end of medulla 75%-90% of fibres cross over to opposite side to form the lateral corticospinal tract in the spinal cord. The 10% fibres that doesn’t cross over to opposite side form the anterior corticospinal tract in the ventral funiculus of spinal cord. Most of these fibres cross over to opposite side at the lower segmental levels as they further descent in anterior column of spinal cord. About 2% of fibres remain ipsilateral known as the bundle of Barnes and supply axial muscles of trunk and proximal limb.
The corticobulbar fibres arise from lower third of motor homunculus and descends in corona radiata and genu of internal capsule to reach brainstem. In the midbrain it is in the medial part of cerebral peduncle and in basis pontis it is intermixed with corticospinal tract. All motor cranial nerves receives corticobulbar fibres from bilateral motor cortex except lower part of face which receives corticobulbar fibres only from contralateral motor cortex. That is why lower part of opposite face alone is affected in lesion involving motor cortex, corona radiata or internal capsule. The other cranial nerves are spared as they get 50% of their fibres from the unaffected side. So a patient with right internal capsule lesion will have left hemiplegia with left upper motor neuron facial palsy as the lower face gets it upper motor neuron only from opposite side. The left lower part of face alone is affected and the facial palsy is on the same side of hemiplegia and facial deviation is to the opposite side of hemiplegia. The eye closure will be normal as the upper part has bilateral representation. All other motor cranial nerves loose 50% of their upper motor innervation but they will be asymptomatic as the rest 50% takes up the function.
So what are the possible sites of localization of hemiplegia?
In hemiplegia the functional deficit is obvious. The patient will tell that he has weakness of one side. The various sites for localization of hemiplegia include
Motor cortex of opposite side
Corona radiata of opposite side
Internal capsule of opposite side
Brainstem of oppose side including midbrain, pons and medulla
Cervical cord- C1-C5 on the same side
Ipsilateral cervical cord causing hemiplegia is very rare. This is because ischemia, one of the common etiology will not cause hemiplegia in cervical cord as a single central anterior spinal artery supply both sides. Rarely unilateral demyelination or compressive lesion can produce
Ipsilateral hemiparesis. Absent facial deviation is the clue. Absent facial deviation need not always be a cervical cord lesion. Medullary lesions and lesions in corona radiata can spare facial fibers. Respiratory weakness and decreased sensation in c2, c3 dermatomes are other clues of a cervical cord involvement. Cervical cord lesion producing hemiplegia is very rare and need not be considered routinely in the differential.
Brainstem
A brainstem lesion causing hemiplegia produces a crossed hemiplegia. This means cranial nerve palsy on the side of lesion and hemiplegia on the opposite side as the corticospinal tract fibers cross over to opposite side at the lower part of medulla. The location in brainstem is determined by which cranial nerve is involved.
Midbrain- 3rd and 4th
PONS- 5,6,7,8
Medulla- 9,10, 12
The side is determined by which side the cranial nerve is involved and hemiplegia will be on opposite side.
So, a Right Midbrain lesion will cause right 3rd CN palsy with Left hemiplegia
Similarly if a patient has right 12th cn involvement and left hemiplegia. The hemiplegia is crossed as cn is on one side and hemiplegia is on opposite side suggesting that it is a brainstem lesion. The lesion is in medulla as 12th cn nucleus is in medulla. It will be in right medulla as 12 th is involved on the right side and hemiplegia will be on opposite side
Motor cortex
Motor cortex lesion will produce hemiplegia and UMN facial palsy of opposite side along with cortical features. The main cortical features include aphasia with left cortical lesion and inattention and neglect with right cortex lesion. Aphasia is a language dysfunction where patient will have difficulty with speech comprehension, fluency, naming, repetition, reading and writing. Neglect and inattention are acquired asymmetry in the processing of information from one side of the body or space. A patient with sensory inattention will perceive stimuli when touched on right and left side separately but on touching both sides simultaneously will perceive stimuli from right side only.
Right hemiplegia with right UMN facial palsy along with aphasia suggest a left cortical lesion.
Left hemiplegia with left UMN facial palsy and left side neglect suggest right cortical lesion
Other cortical features include
Anosognosia
Apraxia
Acalculia
Cortical sensory loss
Prosopagnosia
Visual agnosia etc. which we will discuss in detail when we discuss the functions of various lobes of the brain.
If the patient has no cortical features or crossed cranial nerve palsy the lesion is in either internal capsule or corona radiata
In Internal capsule lesion patient will have hemiplegia and UMN facial palsy of opposite side.
The weakness will be proportionate in upper and lower limb which means the grade of weakness is same in upper limb and lower limb. This is because the corticospinal fibers are compactly packed in ant 2/3 of post limb of internal capsule and a small lesion there will affect all fibers equally
There won’t be any cortical features or CN involvement other than opposite side UMN facial palsy
Right IC lesion will produce left hemiplegia with equal weakness in upper limb and lower limb with left UMN facial palsy with facial deviation to right and left eye closure normal
In Corona radiata lesion patient will have hemiplegia and UMN facial palsy of opposite side.
There won’t be any cortical features or CN involvement other than opposite side UMN facial palsy. It’s different from internal capsule in that there is disproportionate weakness in upper and lower limbs, that means weakness grade is different in upper limb and lower limb since the CST fibers are widely separated in corona radiata unlike in internal capsule where they are very close to each other. A small lesion is more likely to involve some fibers more than other in corona radiata.
Right CR lesion will produce left hemiplegia with left UMN facial palsy with facial deviation to right and left eye closure normal. The weakness will be more in upper limbs than lower limb or vise versa
Aetiology
Once you know the anatomical site of localization of hemiplegia the next step is to identify the aetiology. Other concurrent illness, temporal evolution of disease and past history often gives a clue to the aetiology. For example acute onset hemiplegia in a patient with multiple vascular risk factor suggest a stroke. Sub acutely involving hemiplegia in a patient with past history of brain tumour may suggest a recurrence. A waxing and waning hemiplegia in an elderly with recent fall may suggest a subdural hematoma. Stroke is the commonest cause for acute onset hemiplegia and it can be due to thrombosis of blood vessel, haemorrhage or embolism. An early morning stroke which evolves over few hours in a patient with multiple risk factors may suggest an ischemic stroke due thrombosis. An acute onset hemiplegia when patient is straining associated with headache may suggest a bleed. An hemiplegia which is maximum at onset and improving rapidly in a patient with risk factor like AF or valvular heart disease suggest an embolic stroke. Though history can give a clue an imaging is often required to confirm the aetiology . The imaging will also help to check whether our anatomical localization from history and physical examination is correct
Before we finish lets revise what we discussed in this session. In a hemiplegia the patient will tell the functional deficit. The anatomical sites of localization include motor cortex, corona radiata, internal capsule and brainstem of opposite side of the body. If the patient has cortical features like aphasia or neglect the localization is in motor cortex. If the patient has a crossed cranial nerve palsy the localisation is in brainstem. It there are no cortical features or cranial nerve involvement other than UMN facial paly on the same side of hemiplegia the localization is in internal capsule or corona radiata. If the hemiplegia is proportionate with equal involvement of upper and lower limb the localization is in internal capsule and if its disproportionate with upper limb more than lower limb or vice versa the localization is in corona radiata.
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