The Descending Tracts (Motor) Tract Origin Decussation Destination Functions

Lateral Tracts travel within the lateral column of the spinal cord. Voluntary movements distal musculature. Cortical control Corticospinal Motor cortex Almost all fibres, 80% Alpha LMN in ventral Conscious voluntary Precentral gyrus in medulla. horn; many via muscle control. Rapid monosynaptic pathways. skilled movements, predominantly in limbs. Rubrospinal Red nucleus. All fibres, most at level Alpha and gamma LMN Influences tone of limb of origin in midbrain. in ventral horn. muscles, excitatory to flexors and inhibitory to extensors. Venteromedial tracts travel within venteromedial column of spinal cord. Posture and locomotion under brain stem control. Tectospinal Superior colliculus of All fibres, in midbrain, Alpha and gamma Influences reflex midbrain. close to level of origin motorneurones in ventral postural movements horn, mainly cervical. related to visual stimuli. Vestibulospinal Vestibular nuclei of None. Alpha and gamma Balance and posture pons and medulla motorneurones in ventral reflex postural horn. movements, excitatory to extensors and inhibitory to flexors. Reticulospinal Pontine and medullary Pontine mainly Alpha and gamma Influence voluntary reticular formation. uncrossed, medullary motorneurones in ventral movement and reflex widely dispersed groups mixed . horn. activity, particularly of of cells. proximal joints and axial musculature.

Descending Tract Lesions Pyramidal (corticospinal) tract lesions Loss of fine skilled movements. Babinski sign present. NB.Also present as a normal feature in first year of life. Superficial abdominal reflex absent. Cremasteric reflex absent. Signs contralateral, ipsilateral or bilateral dependent on level of lesion.

Extrapyramidal tract lesions Paresis / Paralysis. No muscle wasting other than that due to disuse. Hypertonicity (spasticity), involving predominantly flexors in upper limb and extensors in lower limb, develops over several days. Hyperreflexia develops over several days. Clasp knife rigidity. Clonus. Signs contralateral, ipsilateral or bilateral dependent on level of lesion.

Lower motor neurone lesions Paresis / Paralysis. Muscle atrophy. Fasciculation. Hypotonicity (flaccidity). Hyporeflexia / Areflexia.

In actual clinical practice the pyramidal and extrapyramidal features of UMN lesions occur together. Lesions of the basal ganglia and cerebellum are often described as extrapyramidal but differ from UMN lesions in not involving descending tracts which influence motorneurones directly or via spinal interneurones. Lesion in the Internal Capsule (hemorrhagic, embolic infarct) can cause problems as corticospinal tract passes through here the rubrospinal tract may take over functions after a few months leading to almost full recovery from (e.g.) CVA
Spinal Shock Syndrome of depression or loss of all cord function below lesion following acute severe damage to spinal cord. Flaccid paralysis below level of lesion. Hyporeflexia / areflexia below level of lesion. Sensory loss below level of lesion. Hypotension from loss of sympathetic tone if lesion is at high level. Duration up to one month. As shock resolves spinal neurones regain activity, upper motorneurone signs develop and some recovery of sensation occurs below level of lesion.

The Ascending Tracts (Sensory)

Tract Lateral Spinothalamic Origin Free nerve endings. A(fast) and C(slow) fibres. Synapse in dorsal horn (substantia gelatinosa). Various receptors. Synapse in dorsal horn (substantia gelatinosa). Meissner`s corpuscles (two point discrimination); Pacinian corpuscles (vibration); muscle, tendon and joint receptors (proprioception). Synapse in nuclei gracilis and cuneatus Muscle, tendon and joint receptors Synapse in nucleus dorsalis (Clark`s column).. Decussation In spinal cord, within one segment Then travels in spinal lemniscus Destination Thalamic synapse in ventral posterolateral nucleus. Posterior limb of internal capsule. Thalamic synapse in ventral posterolateral nucleus Posterior limb of internal capsule. Thalamic synapse in ventral posterolateral nucleus. Posterior limb of internal capsule. Function Pain and temperature Somatotopic representation in cortex.

Anterior spinothalamic

In spinal cord over several segments Then travels in spinal lemniscus Brain stem Enters medial lemniscus

Crude touch and pressure Somatotopic representation in cortex. Discriminatory Touch, Vibration Concious Proprioception

Dorsal columns

anterior and posterior spinocerebellar tracts

Posterior tract uncrossed and enters inferior cerebellar peduncle on way to cerebellar cortex. Anterior tract mainly crosses at level of synapse and enters superior cerebellar peduncle on way to cerebellar cortex. Crossed fibres recross via middle cerebellar peduncles.

No third order neurone Info not at conscious level

Unconscious Proprioception

Blood Supply Anterior cerebral

Middle cerebral

Posterior cerebral

Anterior cerebral

Posterior cerebral

Lesions Head Trauma - Brain Concussion Reversible impairment of neurological function. o Duration minutes to hours. o Mechanism unknown. o Imaging normal. May be followed by post-concussive syndrome of headache etc. Diffuse axonal shear injury Haemorrhage (see below) Contusion Occurs where cerebral hemispheres abut ridges of bony skull eg. frontal, temporal and occipital poles. May be coup or contre-coup (see pic right) Cerebral oedema

Extradural haemorrhage: Bleeding from a torn middle meningeal artery between the dura and the bone of the skull. Typical history: Injury to head Loss of consciousness for a short time Lucid period lasting hours days (as pressure builds up within the skull) Drowsiness, coma, death if no intervention Diagnosed by CT or MRI. Subdural haemorrhage: Bleeding from a torn cerebral vein between the dura mata and arachnoid mata. Typical history: Injury to head a long time ago, may have been trivial. Days months pass (as pressure builds up slowly within the skull) Headache, drowsiness and confusion Possible hemiparesis / sensory loss Coma, death if no intervention (or may resolve on their own) Diagnosed by CT or MRI. Subarachnoid haemorrhage: Bleeding from a torn cerebral artery into the subarachnoid space. Typical history: Usually no injury mostly from Berry aneurysm Sudden onset intense headache with stiff neck (as aneurysm bursts). Possible papilloedema and retinal haemorrhage Usually vomiting, possible loss of consciousness for hours days Diagnosed by CT or MRI. Intraparenchymal haemorrhage: Within brain substance. Spontaneous form results from hypertension, tumours, vascular malformations, coagulation defects, mycotic aneurysms, etc. Typical history Traumatic form is associated with other head trauma. Symptoms/signs depend on site and extent of bleed. Diagnosed by CT or MRI.

Ishaemia and infarction Thrombotic infarct occurs in association with atherosclerotic plaque. Embolic infarct occlusion of vessel by emboli of: a) blood clot from heart or proximal artery. b) septic focus. c) air. d) fat. Transient ischaemic attack (TIA) neurological episode lasting minutes. ? Involves infarction. Symptoms/signs depend on site and extent of lesion. Diagnosed by CT or MRI. Transient Ischaemic Attack (TIA): A cerebrovascular event usually caused by micro-embolus and resulting in a transient ischaemia with results that resolve within 24 hours. Stroke: A cerebrovascular event usually (80%) caused by embolus resulting in an infarct with results that may resolve days months. Haemorrhagic causes of strokes are far less common (15%). Most common sites for thrombi or atherosclerotic plaques resulting in strokes or TIAs: Subclavian just after it branches from aorta Common carotid just after it branches from aorta Vertebral just after it branches from subclavian Internal carotid just after it branches from common carotid The internal capsule (links the cortex to the brain stem) is one of the most commonly affected areas in a stroke the following may be seen: Contralateral limb weakness developing over hours Contralateral hemiplegia / hemiparesis Apahasia if the dominant side is affected Weakness of one side of the face

Some important Fractures Skull base fracture (of Sphenoid, temporal and occipital bones - middle cranial fossa floor) CSF otorrhoea if meninges superior to middle ear and tympanic membrane ruptured Danger of CSF infection Assessment clinical and CT.

Skull base fracture (of anterior cranial fossa floor including Frontal and ethmoid bones (cribriform plate of ethmoid) Symptoms/signs related to associated facial and brain injury; anosmia; CSF rhinorrhoea Danger of CSF infection (should not blow nose) Assessment clinical and CT.

Facial Skeleton Fractures External Nose Nasal bones and septal cartilage involved. Symptoms/signs cosmetic and functional. Assessment clinical; imaging usually unhelpful. Zygomatic Arch Zygomatic, maxilla and temporal bones involved. Symptoms/signs mainly cosmetic. Assessment clinical, plain X-ray and CT. Maxilla Ethmoid, nasal, zygomatic, palatine and sphenoid bones may also be involved.

Le Fort classification. Symptoms/signs cosmetic and functional. Assessment clinical and CT.

Mandible Mandible and temporo-mandibular joint involved. Symptoms/signs functional. Assessment ortho-pantomography (OPG) and CT. Blowout Fracture (intraorbital fracture): Caused by an indirect traumatic injury (e.g. tennis ball) onto the orbit. The sudden rise in pressure within the orbit can cause the thin bone here to fracture. Usually this is a trapdoor fracture in the inferior part of the orbit as this is the weakest area. Fat is displaced into the fracture line this is not a serious consequence. There is a possibility that inferior rectus will become displaced into the fracture line and caught. If this occurs o Patient will be unable to look up without pain o Patient will be unable to look down without diplopia Surgical correction is needed quickly or the problem becomes unresolvable due to damage to the muscle May also result in introrbital bleeding and exophthalmos

Skull Vault Fractures Frontal, parietal, squamous temporal and occipital bones involved. Fracture simple or depressed. Symptoms/signs mainly related to associated brain injury. Assessment plain X-rays and CT.

Epilepsy Epilepsy has a high prevalence of 5% (1 in 20) with the most chance of occurring in the very young and very old. It is caused by a change in the excitability of neurones, which may result from: meningitis, stroke, trauma or heritable channelopathies. Types of seizure Complex partial seizure: Abnormal discharge occurs from a focus and spreads locally across a limited area. The patient may seem fully aware but there is an altered state of consciousness. Symptoms include automatisms (chewing, swallowing etc). Prior to onset the patient may experience warning signals: dj vu or jemais vu may result from involvement of the hippocampus (memory) while perceptual changes or auras may arise from involvement of sensory areas. These are generally temporal lobe in origin and may progress to generalised seizures. Partial with secondary generalised: This starts as a simple partial seizure with temporal foci often associated with perceptual changes or auras. Generally there is activation of a more central focus and whole brain (generalised) involvement. With frontal foci there are motor seizures a stiffness and jerking of the limbs (Jacksonian seizure). Occipital seizures generally preceded by hallucinations of light / colour. Absence seizure (generalised): this is part of the generalised spectrum. It is rare in adults, starting in the 6-12 year range with more girls than boys affected. The patient seems to switch off and cannot be alerted or woken up. Responds well to anti-epileptics. Generalised tonic-clonic: There is whole brain involvement and so no warning. In the tonic phase the whole body stiffens, breathing may stop, and there is a loss of bladder control. In the clonic phase there are muscle jerks. This is followed by loss of consciousness and muscle relaxation. When consciousness returns, sleepyness, headache and aching limbs are common there is usually no memory of the episode.

Pharm: Na+ Channel blockers Phenytoin, carbamazapine Block the Na+ channel in its inactivated state they are therefore use-dependent. Only when the Na+ channel pool is rapidly used up (seizure) will the slow recovery time matter. Aphasia Type Brocas Wernikes Lesion

Pharm: GABA (Cl- channel) agonists Benzodiazepines (e.g diazepam), barbiturates (e.g phenobarbitone) The GABA channels inhibit neuronal fireing when activated they do this by letting in Cl- which hyperpolarizes the cell.

Other: Removal of abberent areas guided by MRI Implant: vagal nerve stimulation

Speech Non-fluent, no grammar Fluent, grammatical, but meningless

Comprehension Good but not perfect Poor

Other features Impaired repetition and paraphasic errors Impaired repetition and greater paraphasic errors

Motor association cortex of frontal lobe Posterior frontal lobe

Brocas area may be involved in making grammatical sentences out of words, or may contain memories for fine series of motor controls required for articulating word sounds Aprosodias are inabilities in the understanding of emotional emphases

Consciousness: Requires The reticular formation of the brainstem (spread through pons and medulla) responsible for wakefulness. The limbic system responsible for affect, mood, attention and motivation. The cerebral cortex responsible for state of awareness and for interaction with the environment. Levels of consciousness Normal fully oriented in place, time and person. Lethargy (Somnolence; Sleepiness) awareness impaired but may become normal or nearly so on arousal; speech slow; voluntary movements diminished and slow; EEG mildly abnormal with some sleep pattern. Stupor no real awareness; speech only in response to pain; voluntary movements minimal or there may be mass movements in response to pain; EEG abnormal but distinguishable from normal sleep pattern. Coma (Unconsciousness) no awareness; speech absent; movements absent or only reflex in response to pain; EEG grossly abnormal or absent. Persistent Vegetative State Reticular formation intact but cerebral cortex non-functional. Person is awake, ie. eyes are open and move around and sleep-awake cycles are present. Awareness is absent. Response to verbal command or pain is absent. EEG contains rhythmic activity resembling sleep cycles.
Eye Opening Spontaneous to speech to pain no response Best Motor Response Obeys Localizes pain pushes your hand away Flexion-withdrawal moves away from the pain Flexion-abnormal upper and lower limbs flex Extension upper and lower limbs extend no response Best Verbal Response Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds no response E 4 3 2 1 M 6 5 4 3 2 1 V 5 4 3 2 1 The Glasgow Coma Scale (left) E + M + V = 3 to 15 90% less than or equal to 8 are in coma Greater than or equal to 9 not in coma 8 is the critical score Less than or equal to 8 at 6 hours - 50% die 9-11 = moderate severity Greater than or equal to 12 = minor injury Coma is defined as: Not opening eyes Not obeying commands Not uttering understandable words.

What physiologically produces coma? Damage to brain stem reticular formation. Extensive cortical damage, especially if bilateral, but sometimes involving only the dominant hemisphere. Supratentorial lesion usually tumour or haemorrhage not due to infarc the area covered by an infact is not sufficient. Infratentorial lesion tumour, haemorrhage or infarction (affects the reticular formation of the brainstem) Toxic/Metabolic disorders infection, drugs, diabetes, uraemia, etc.

Subfalcine

Transtentorial Central Intracranial mass lesions Cause compression and destruction of the brain adjacent to a lesion the expansion of this lesion causes a rise in intracranial pressure. This in turn may displace a structure from one place or compartment to another this is called herniation (see diagram)

Types of herniation Subfalcine: the anterior cerebral artery may be compressed Transtentorial: compresses the brainstem Tonsillar: the tonsils of the cerebellum are pushed through the foramen magnum

Tonsillar

Central: the brainstem may be pushed towards the foramen magnum nerves may be compressed (esp CNIII causes papillary signs).

Compensation Blood, CSF and the brain itself are incompressible substances. If an expansile mass is present the only way to compensate for this is to reduce the levels of intracranial blood and CSF. This works well for small lesions but larger lesions may overcome this compensation this problem is compounded by brain oedema. As the intracranial pressure rises, the cerebral perfusion drops. This is compensated by a rise in systemic blood pressure and a reflex tachycardia occurs also. Symptoms of mass lesions include: headache, N&V (pressure on vomiting center), altered mental state, papilloedema, visual loss (pressure on optic chiasm / tract etc.) and irregular respiration. Death usually occurs through ischaemia as blood flow drops.