Neuroscience Essays

1. Describe the major sensory pathways that provide input to the somatosensory cortex and outline their functions.
What would be the effect on each caused by a lesion of the left side of the spinal cord at C4?

2. Define epilepsy, describe how seizures are classified and discuss the therapeutic approaches that are used to
control the disease.

3. Describe the functional organization of the visual pathways in the nervous system and give examples of how vision
is affected by damage to these pathways.

Approx. 800 words

1.
Major sensory pathways allow sensory information about the bodies internal and external environment to be carried to the CNS.
Information is carried via afferent nerve fibres to the primary somatosensory cortex, located in the postcentral gyrus in the
parietal lobe. Varying modalities such as touch, pressure, pain and touch are carried to the somatosensory cortex where these
sensations are consciously perceived. I will be explaining the different types of major sensory pathways that provide input to the
somatosensory cortex and explain the consequences of a lesion to the left side of the spinal cord at the level of C4.

The major sensory pathways I will be explaining today are: the dorsal column-medial lemniscus pathway (DCML), the
spinothalamic pathway, and the spinoreticulothalamic pathway. These pathways can also be referred to as ascending tracts and
consist of a sequence of three neurones; 1st order neurone, 2nd order neurone, and a 3rd order neurone. The 1st order neurone
carries information from the receptors to the spinal cord, its cell body lies within the dorsal root.

The DCML pathway is a conscious sensory pathway, carrying information about fine touch, vibration and proprioception from
mechanoreceptors to the somatosensory cortex. They are located on the dorsal column of the spinal cord and consist of two
tracts; the fasiculatus cuneatus and the fasiculatus gracilis. First order neurones of both tracts enter the dorsal root of the spinal
cord carrying information from the ipsilateral side of the body. The fasiculatus cuneatus pathway carries information from the
upper limb to the medulla oblongata where it synapses with the cuneate nucleus (of the medulla oblongata). Whereas the
fasiculatus gracilis which lies in the medial part of dorsal column and carries information from the lower limb towards to the
medulla oblongata where it synapses with the gracile nucleus. Second order neurones then start from either the cuneate or
gracile nucleus, these fibres then decussate at the level of the medulla oblongata (now travelling contralaterally) forming the
medial lemniscus which synapses at the ventral posterolateral nucleus (VPN) of the thalamus. Third order neurones starting from
the VPN of the thalamus ascend through the internal capsule and terminate at the primary somatosensory cortex of the brain.
(Figure 1)

The second sensory pathway I will be outlining is the spinothalamic pathway. This pathway is split into two separate tracts; the
anterior spinothalamic tract which carries sensory modalities of crude touch and pressure, and the lateral spinothalamic tract
carrying information about pain and temperature. First order neurones enter spinal cord and synapse at the tip of the dorsal
horn (grey matter) in an area known as the substantia gelatinosa. Second order neurones then decussate about 1-2 segments
above point of entry and ascend via the spinothalamic tracts; either anterior or lateral depending on type of modality. Second
order axons then synapse in the VPN of the thalamus. Third order neurones then ascend via the internal capsule and terminate
in the somatosensory cortex. (Figure 2)

Another sensory pathway which is evolutionary older than the others mentioned previously is the spinoreticulothalamic
pathway. Associated with the carrying nociceptive information, and responsible for the slow and dull aching pain. The nerve
fibres of this pathway are unmyelinated. Instead of having a sequence of three neurones this tract has four. The first order
neurone enters the spinal cord and synapses. The second order neurone then decussates within the spinal cord and ascends and
synapses in the reticular formation in the medulla, pons and midbrain. The third order neurone then ascends to the thalamus
where it synapses with the fourth order neurone travelling to the somatosensory cortex. The functions of this tract are still not
clear but many theorise that it is responsible for the slow dull aching pain from visceral sources?

Lesions to the spinal cord can therefore affect these pathways, resulting in a number of consequences to a patients sensory
functions. The effect of left sided lesion at C4 will depend on where the tract decussates. A patient with this type of lesion may
present with loss of sensation of fine touch, vibration and proprioception of the upper and lower limbs on the left side. The
pathway affected in this case is the DCML tract, as the location of the lesion is below the level of decussation the ipsilateral side
is affected. The Rombergs test may be used to test for the normal function of this tract. The patient may also exhibit loss of
sensation of crude touch, temperature and pain on the right-hand side a few spinal segments below actual site of lesion. The
spinothalamic pathway is affected in this case, since fibres decussate within the spinal cord the contralateral side of the body is
affected in relation to the site of the lesion.

In this essay, I have outlined the different types of sensory pathways leading to the somatosensory cortex of the brain which
allow us to consciously perceive sensory information from relayed from various sensory receptors. The pathway which carries
information regarding crude touch, pressure and proprioception is the DCML pathway, whilst the pathway conveying pain and
temperature is the spinothalamic pathway. An additional pathway thought to be responsible for the slow dull aching pain we
experience is the spinoreticulothalamic pathway, an evolutionary older pathway. The implications of a lesion to the spinal cord
have also been discussed highlighting the importance of these pathways to our perception of out sensory environment.
2.
Epilepsy is a neurological condition characterised by the tendency to have recurrent unprovoked seizures. It is one of the most
common neurological disease and affects approximately 400000 people in the UK. I will be outlining the symptoms, causes and
risk factors of epilepsy. Focusing on the classification of different types of seizures and the therapeutic treatments currently
available to control the condition.

Epilepsy is a common neurological condition often defined as the propensity of having recurrent unprovoked seizures. A seizure
can be defined as an abnormal paroxysmal synchronous discharge of a large number of neurones. The condition affects around
0.6% of the population, with there being a higher prevalence in the developing world. The causes of many cases of epilepsy are
unknown, and it is stated that about 50% of new onset cases of epilepsy in adults is never explained. However sometimes
epilepsy can be an underlying symptom of trauma (leading to brain damage), tumours, stroke, infection and other kinds of
neurological diseases. Recently some genetic mutations have been linked to the development of epilepsy, such as the KCNQ2/3
gene thought to be associated with benign febrile epilepsy. There are also certain risk factors associated with epilepsy, such as
known neurological disease, cerebrovascular disease, family history, previous head injury, substance misuse and abnormal
neurological development. The presentation of epilepsy will depend on multiple factors, first being the CNS region at which the
abnormal electrical activity occurs, then if this electrical activity spreads to other parts of the CNS.

The diagnosis of epilepsy can be difficult due to sudden and uncontrollable nature of the condition therefore a detailed history
with witness accounts is essential. Investigative techniques such as electroencephalograph (EEG) and MRI may be used in order
aid with the diagnosis. EEG can be used to measure abnormal electrical activity at the scalp, allows for the detection of any
abnormal synchronous neuronal firing through the neuronal networks. MRI can also be useful in detecting structural
abnormalities which may be causing epilepsy, such as hippocampal sclerosis or a brain tumour.

As the clinical presentation of epilepsy can be varied between many individuals it is then very useful if we can categorised certain
symptoms, classification of these symptoms can therefore aid in effective management of epilepsy. Seizures are classified into
either focal or generalised seizures. Focal or partial seizures originate form one part of the brain and is limited to one hemisphere
or even one region of the brain. Therefore symptoms can vary depending on which part of the brain is affected, for example if
the motor cortex was involved then involuntary muscle contractions may occur. Generalised seizures originate from one area and
spread rapidly throughout the brain, involving both hemispheres of the brain. These seizures are further divided into; tonic-
clonic, absence, clonic, tonic, atonic and myoclonic. In a tonic-clonic seizure after the initial loss of consciousness has two phases;
the tonic phase where the body becomes rigid and stiff, followed by the clonic phase where the body violently jerks and spasms
sometimes even involving micturition. The patient may then slowly start to regain consciousness a few minutes after the seizures
has started. Another type of generalised seizures is an absence seizure which is mainly seen in children. It is usually noticed by
parents or carers because the child will suddenly stop talking mid-sentence or stop their physical activity altogether and stare off
into space. The patient themselves are unaware of this and usually recover quite rapidly. Atonic seizures are seizures where there
is a sudden loss of muscle tone resulting in the patient collapsing to the floor, recovery from this type of seizure is also very rapid.
Myoclonic seizures involve the involuntary jerking or twitching of muscles, any part of the body can be involved but usually the
limbs and facial muscle are the most commonly affected. Seizures can also be classified depending on the impairment to
consciousness, if the patient remains conscious or aware then this is termed as a simple seizure. If, however, the patient loses
consciousness then this is referred to as a complex partial seizure. Usually seizures are self-limiting and resolve with time,
however prolonged seizures is a medical emergency which may require interventions to stop them, this is called status
epilepticus.

Drugs used to treat epilepsy are referred to as anti-epileptics or anti-convulsants, they work by inhibiting the abnormal
paroxysmal synchronous discharge often responsible for the seizure. The main actions of these drugs are to increase the activity
of inhibitory GABA systems, inhibit voltage gated sodium channels and inhibit voltage gated calcium channels. These drugs do
not treat the underlying cause but do prevent the patient from having further seizures in the future. As mentioned previously the
classification of seizures allows clinicians to plan the most effective ways to manage epilepsy. For tonic-clonic, partial, temporal
seizures then drugs that enhance GABA activity would be given such as benzodiazepams like diazepam and clonazepam, thse
bind to the GABAA receptor and increase the receptors affinity for GABA. These drugs administered intravenously to treat status
epilepticus. Due the potency of these drugs they are not usually given to treat epilepsy, however they are sometimes given in
epilepsy which hasnt responded to previous drug treatment. Baribiturates like phenobarbitone prolong the time that GABA
activated calcium channels stay open. Vigabatrin inhibit GABA transaminase therefore preventing the breakdown of GABA, whilst
tiagabin inhibits the uptake of GABA hence increasing the concentration of GABA in extracellular space. Drugs that block voltage
gated sodium channels include carbamazepine and phenytoin, these reduce the frequency of action potential firing.

As for treating absence seizures, drugs like ethosuximide are used which block voltage gated calcium channels in the thalamic
neuron. Drugs like lamotrigine and sodium valproate can be used to treat both tonic-clonic and absence seizures, lamotrigine
blocks sodium channels whilst the later is suggested to work by bloking voltage gated sodium channels. Other drugs used to treat
epilepsy include gabapentin and pregabalin, whose mechanism is uncertain. Retigabine which provoke potassium channels of
KCNQ type suggesting it may work by stabilising membrane potential. Perampanel and felbamate, which act as antagonists of
AMPA receptors. Levetiracetam binds to synaptic vesicle protein SV2A which affects NTransmission. Other non-pharmalogical
treatment include ketogenic diet, this is more of a conventional therapy as it is not sufficiently effective). Vagal stimulation,
where a surgical device stimulates the vagus nerve via regular electrical stimuli. Surgery, to remove tissue which may be
exacerbating the abnormal electrical activity.

3.
The ability of sight is essential to our daily lives, whilst on the surface it seems like something we take for granted the processing
of our visual environment is a very complicated process. Information from the retina must reach the visual cortex of the brain. I
will be describing the functional organisation of visual pathways in the nervous system and will explain vision is affected if these
visual pathways are damaged in anyway.

Photoreceptors present on the retina convert light waves into visual information, retinal ganglion cells receive this information
and relay it the visual cortex located in the occipital lobe of the brain. There are around four types of photoreceptors; the rod
cells which are very sensitive and allow for vision at low light levels. Cone cells of which there are three types that differ
according to wavelength sensitivities of photopigment. The fovea is where there is the highest density of cone cells. These
photoreceptor cells are connected to bipolar cells which are then connected to retinal ganglion cells. Therefore the sequence of
information passes from photoreceptor to bipolar cell to ganglion cell whoms axons form the optic nerve.

As humans, we have a binocular visual field seen by both eyes, different areas of the visual field are viewed by different parts of
the retina. The left visual field is viewed by the nasal retina of the L eye and the temporal retina of the right eye. The right visual
field is viewed by the temporal retina of the left eye and the nasal retina of the right eye (figure 1). Monocular regions, only seen
by one eye, are viewed by the nasal region of the left and right eye respectively. Axons of retinal ganglion cells from one eye are
contained within the optic nerve, therefore the optic nerve contains information from both the nasal and temporal retina of one
eye. The optic nerves from both eyes decussate at the optic chiasm into theyre corresponding optic tracts as follows; nasal axons
project into contralateral optic tracts and temporal axons project into ipsilateral optic tracts. This results in each optic tract
containing axons from the nasal retina of the opposite eye and the temporal retina of the ipsilateral eye, e.g. the right optic tract
contains axons from the left nasal retina and the right temporal retina. Therefore the brain receives information from both eyes
about contralateral half of visual field. The optic tracts project then project to the lateral geniculate nucleus of the thalamus
where they synapse. Neurons then leave the LGN as optic radiations. These optic radiations then project to the primary visual
cortex located in the occipital lobe of the brain. Within the primary visual cortex information passes through cerina areas of the
cortex, these being referred to as higher visual centres. Information first passes through V1 or area 17 to V2, this is where the
majo streams diverge. Cognitive stream of what passes to V4(area 19) then to inferior temporal cortex (area 37). Motor stream
of where passes to medial temporal area V5 (area 7a). Termination of both of these streams allows for the perception of the
visual field.

Lesions or damage to the visual pathway can have major consequences to vision. Differing effects can occur depending on the
where the lesion occurs. Lesions of the optic nerve results in monocular blindness or anopsia of the eye on the side affected e.g.
left optic nerve damage results in left anopsia. Lesions of the optic chiasm will cause bitemporal heminopias, lesiosn or damage
here would disrupt the axons decussating. As these axons carry information about both temporal visual fields, it results in deficits
in the temporal hemifields, a likely cause of this is a pituitary tumour. Lesions to the optic tract will result in contralateral
homonymous hemianopia, blindness of half of the visual field. Therefore, a lesion or compression of the left optic tract will cause
information from the nasal retina of the right eye and the temporal region of the left eye to be blocked, as these carry
information about the right half of the visual field, this area of the visual field will be lost.

Lesions to the optic radiations can cause quadrantanopia and hemianopias. The optic radiations from the LGN and can be divided
into two; the dorsomedial bundle which carries fibres of the lower quadrant and the ventrolateral bundle which carries fibres of
the upper quadrant. Therefore, lesions of either one of these bundles will result in deficits in one of the quadrants of the visual
field or a quadrantanopia. Complete lesions of the optic radiations on one side will result in vision loss in half of the visual field
(homonymous hemianopia). E.g. if the left optic radiations were lesioned, the temporal visual field of the left eye and the nasal
part of the right eye will be lost. This is like the effect of a lesion to the optic tracts, in which a lesion will also result in
homonymous hemianopia.

Damage to the visual pathways can also cause defects in the pupillary light reflex, this can be used as a diagnostic tool for lesions.
If the right optic nerve is damage then there is will be a reduced or no direct and consensual response when light is shone in the
right eye, but if light is shone in the left eye then both the direct and consensual response is present e.g. both pupils constrict.
Lesions of the right optic tract which contains information about half of the visual field will cause a reduced but not absent
pupillary light response, as the left optic tract is still intact some information is still being transferred to the brain. Lesions to the
oculomotor nerve leads to ipsilateral loss of the pupillary light reflex, e.g. damaged left oculomotor nerve leads to both the direct
and consensual response in the left eye to be lost.