The nervous system coordinates bodily functions via chemical and electrical signals.
It processes information throughout the body by carrying signals between the central nervous system (CNS) and peripheral nervous system (PNS). The CNS is composed of the brain and spinal cord, while the PNS consists of nerves which are connected to the CNS and reach the rest of the body.
The nervous system comprises the somatic (voluntary) nervous system and the autonomic nervous system. The somatic nervous system is the side of the system that deals with commands that we are aware of and can control e.g. the connection between the brain, spinal cord and skeletal muscles. The autonomic nervous system is the side that governs involuntary and reflex functions such as blood vessel dilation and heart rate.
The spinal cord consists of a central canal filled with cerebrospinal fluid, and grey (H shape) and white matter. Nerves connect to the cord, while the meninges act to protect the cord (alongside the brain).
The brain has several key parts: the medulla oblongata, the cerebellum, the cerebrum and the hypothalamus.
The cerebrum is the uppermost part of the brain that contains many different lobes that control various voluntary functions such as speech, movement and thought.
The hypothalamus includes the anterior pituitary gland, the master gland which secretes different hormones key in metabolism and reproduction, and functions in many systems to regulate sleep, hunger, parental attachment, etc. Its functions include temperature regulation and osmoregulation (blood homeostasis by the kidney).
The cerebellum (“little brain”) controls how movement is executed, although not its initiation. This includes timing of movements, precision, coordination, fine movements and posture. It may also have functions in cognition such as attention and language.
The medulla oblongata is a key part of the brain whose function lies in controlling many autonomous functions including breathing, heart rate, vomiting, blood pressure control, coughing, sneezing and swallowing.
As hinted previously, some functions are voluntary and some are autonomic. This is because the PNS is split into voluntary (somatic) and autonomous systems.
Furthermore, the autonomous system is split into sympathetic and parasympathetic, the two acting antagonistically depending on the situation. They act on all body systems to spark alertness (fight or flight response) in the case of the sympathetic system, or the opposite (rest and digest) by the parasympathetic system. This acts on the pupils (dilation), the respiratory system, circulation, digestion, blood glucose, stress, excretion, etc.
The sympathetic system relies on the secretion of noradrenaline in response to stress, which binds adrenergic receptors to elicit response from the aforementioned systems. Pupils dilate, respiratory rate and heart rate increase, blood pressure increases, digestion is inhibited, etc.
Conversely, the parasympathetic system relies on the neurotransmitter acetylcholine and results in increased digestion, lowered heart rate and blood pressure, glucose storage as glycogen, sexual arousal, excretion, etc.
Let’s delve into the basics of nervous transmission by looking at a motor neurone. Here is the structure of a myelinated motor neurone:
Labelled “insulating sheath”, the myelin sheath is responsible for protecting the electrical impulses that run across the neurone.
Dendrites carry electric signals i.e. nerve impulses towards the cell body (the soma), while the axon carries them away, often towards the receiving dendrites of other neurons.
There are three kinds of neuron: sensory which transmits signals from receptor cells such as those in the eye to the CNS (brain or spinal cord), relay which carries the signal from the sensory neuron and passes it onto a motor neuron which in turn signals the effector tissue to act out the signal e.g. muscle contraction.
These functions give the different types of neuron different structures. Sensory and motor neurons communicate information throughout the body, so have long axons. Relay neurons (a.k.a. interneurons) operate in the CNS and are much smaller. They do, however, have more connections.
The Myelin Sheath
This insulating sheath made up of Schwann cells conducts electricity and therefore is key in ensuring fast signal transmission. The signal is able to “jump” along the axon without losing its strength:
Each pink cell is a Schwann cell. Due to the jump-like action, this conduction is termed saltatory conduction. Factors that affect conduction other than myelination and saltatory conduction (which allow speeds many times faster compared with no myelination) include temperature and axon diameter.
Since chemical movement (kinetic energy) relies on temperature, an optimal temperature maximises conduction. A temperature lower than this would slow it down. This is due to a slower opening of sodium channels for example, and also a slower inactivation resulting in a longer delay.
Axon diameter affects conduction in terms of resistance. The signal travelling along a thin axon encounters the resistance of the axon membrane, while for an axon with larger diameter, a smaller proportion of the signal is met with resistance in this way. The signal carried on the inner section of the axon has no resistance and can travel faster.
What happens in a resting state where no impulses are being sent through a neuron?
This is the resting potential where the membrane permeability differentiates between sodium (Na+) and potassium (K+) ions so that at any given time there are more Na+ ions outside than inside and more K+ ions inside than outside.
According to these electrochemical gradients, Na+ ions should move back inside to balance out their concentration (equilibrate) while K+ ions should move back outside the membrane until the concentrations are equal inside and out. This clearly isn’t the case, so what gives?
Found on the membrane there are Na+/K+ pumps which carry out active transport against the electrochemical gradient of these ions. The resting potential of the membrane is negative on the inside and positive on the outside – but how? Aren’t both sodium and potassium ions positively charged? This is achieved by the pump transferring 3 Na+ ions out while taking only 2 K+ ions in. This is where the difference comes from.
Now we know that in the absence of an action potential the resting potential of the neurone membrane is negative (about -70 mV; millivolts). What precedes an action potential and how does it unfold?
A stimulus may depolarise the membrane by opening up Na+ channels for those ions to rush into the axon. An action potential will occur only if the depolarisation passes a certain threshold. For example, if it reaches -60 mV up from -70 mV it will not trigger an action potential with a threshold of > -45 mV.
Therefore, the power of an action potential is not proportional to that of its stimulus. It either happens or it doesn’t. This is called the all-or-nothing principle.
This is how the voltage of the axon membrane changes during an action potential:
The rush of Na+ ions into the membrane during depolarisation causes the voltage to become positive. Note how only the depolarisation that has passed the threshold initiates an action potential.
Repolarisation occurs when Na+ channels begin to close and K+ channels open, resulting in a rush of K+ ions out of the axon. Before all the K+ channels close, hyperpolarisation occurs which briefly sees the voltage drop below the resting potential level.
This also represents the refractory period where either no stimulus however strong can initiate another action potential (absolute refractory period), or a stimulus slightly greater than usual would be required for an action potential to occur (relative refractory period).
Finally the resting potential is achieved.
Reflex – think of sensory neuron –> interneuron –> motor neuron
The knee-jerk reflex is too famous so it shall be ignored on this occasion (also, what is the point of it anyway? I never recall it saving me from anything, do you?!). Instead we turn to the iris reflex responsible for controlling the amount of light entering your eyes.
(Fun experiment that’s also an opportunity for justified procrastination: go in the bathroom and keep covering an eye and uncovering quickly while staring in the mirror to see how quickly the pupil appears to change size!)
How does this reflex work? Most reflexes have multiple steps, but the outline goes something like this:
receptor –> sensory neuron –> integration centre –> motor neuron –> effector
In other words: the retina (receptor) at the back of the eyes senses the amount of light present. This information is relayed (sensory neuron) to a centre in the brain (integration centre) which then acts upon it by stimulating the motor neuron to carry out a response command to the effector – the iris muscles which contract.
The above example uses the spinal cord as the integration centre instead of the brain. The escape reflex is a haphazard response to an unknown danger, as seen by insects moving in all directions following an attempt to squash them. It can also happen in humans as exemplified by the reflex to pull away from very hot or cold objects, jump at a loud sound or blink when startled by something.
Therefore, the blink, iris and plantar reflexes are used to determine someone’s level of consciousness and nervous system damage.
The iris reflex (pupillary reflex) involves the contraction of the different muscles in the iris when exposed to bright light or dim light. In bright light, the circular muscles contract to make the pupil appear like it contracts. In dim light, the radial muscles in the iris contract, exposing more of the pupil and making it appear like it dilates. The iris reflex helps control the amount of light entering the eye to enable vision.
Both eyes should respond to the light stimulus at the same time, even when just one eye is exposed. A lack of this response indicates problems in the eye’s sensory or motor pathways, or brain stem injury. Therefore, it is a common diagnostic technique in hospital emergency rooms.
The plantar reflex refers to the movement of the toes following an upwards swipe using a blunt instrument from the heel to the top of the foot. The expected movement in healthy adults is for the toes to move downwards, rather than upwards. An upward movement is called the Babinski sign, and indicates underlying nervous system disease. Seen in infants, however, it is normal and represents a primitive reflex.
The blink reflex (a.k.a. corneal reflex) refers to blinking when the cornea is touched. This can be done using a thin piece of cotton wool. Upon contact, the eye should blink instantly. The blink reflex acts to protect the eye against particles or objects that would injure it.
Absence of the blink reflex can help diagnose coma as part of neurological tests.
Investigating reflex times with Student’s t-test
Experiments to investigate changes in reaction time with various factors that affect it, such as alcohol consumption, can be carried out relatively easily. In this experiment, participants had their reaction time measured by e.g. catching a falling ruler, without having consumed alcohol or caffeine; having consumed two different amounts of caffeine (200 and 400 mg) and alcohol; or having consumed two different amounts of caffeine only.
The results show that reaction time was higher to begin with in those who had consumed (unknown amount of) alcohol compared with those who had not. Upon taking caffeine, reaction times decreased in both alcohol and non-alcohol groups. The effect was more pronounced in the alcohol group, but the reaction times were still higher than in the non-alcohol group.
It can be concluded that alcohol slows reaction time, while caffeine speeds it up. Caffeine goes some way to reverse the slowness caused by alcohol, but is still not matched by the caffeine only group.
If we had the raw data for these groups, we could statistically compare the results to establish whether there is a significant difference between the groups e.g. alcohol vs. non-alcohol, 200 mg caffeine vs. 400 mg caffeine, etc.
Student’s t-test is used for data with a normal distribution (single peak with fewer data either side) in order to establish whether there is a significant difference between the means of two linked or independent data groups, or between the mean of one data group and its assumed expected value in the hypothesis. The null hypothesis by default states that there would be no significant difference between data groups.
The result of the test (which can be automatically calculated in software including Excel, SPSS, Matlab, R, etc.) comes with several parameters and values, one of the key ones being the p-value. This represents the probability of there being a difference. Because there isn’t a 100% yes or no answer, all data outcomes are a probability. Commonly, a probability value of 5% or less is used as the threshold for deeming a difference significant.
This means that as long as it is 5% or less probable that these data are indeed different from each other, it will be enough to accept the null hypothesis which stated that there wouldn’t be a difference.
5% is equivalent to 0.05, that is why a p-value of 0.05 is considered the threshold for drawing conclusions regarding the null hypothesis. Often, t-tests will output p-values that are much lower, such as 0.001. Since these values are always probabilities, and thresholds for rejecting versus accepting hypotheses are arbitrary, caution must be taken in how statistical analyses are used in research.
Assessing damage using brain scans
Brain and spinal cord damage can be assessed using a variety of different scans with specific advantages and disadvantages.
Computerised tomography (CT) is a brain imaging technique used for other parts of the body too, which uses X-rays processed by a computer in multiple angles to create a multiple slice picture of the brain. It is used a lot in detecting brain infarction, tumours and haemorrhages.
The issue raised by CT is exposure to radiation which itself can cause cancer.
CT of the spinal cord can reveal the entry and exit points of nerves.
MRI (magnetic resonance imaging) uses magnetic fields and radio waves to build a picture of the atomic emission and absorbance of radio energy following magnetic field exposure (nuclear magnetic resonance, NMR) which results in a picture of a patient’s water and fat locations. It is carried out in a narrow chamber and can be uncomfortable, takes longer to perform than CT and is louder.
Assessment of traumatic brain injury can be carried out over time. The effects can be long-lasting and cause a chain of events, via inflammation, that can result in other symptoms down the line. One of these symptoms is accelerated ageing of the tissue that may result in Alzheimer’s disease. Moderate to severe traumatic brain injury can be assessed prior to scans due to loss of consciousness. Mild injury may cause confusion and short term loss of consciousness.
Stroke occurs when brain tissue is deprived of oxygen due to arteries in the brain becoming blocked, or due to haemorrhage. Initial symptoms include the face dropping, inability to raise arms and hold them raised, and slurred speech. Any of these symptoms immediately indicate that it is time to call an emergency ambulance (F.A.S.T.).
Scans including MRI and CT are carried out in order to assess the extent of the stroke, the location and cause.
Functional magnetic resonance imaging (fMRI) is used moreso in research than medicine, and gives a picture of brain activity based on increased blood flow correlated with neural activity.
This is based on the knowledge that wherever in the brain higher activity takes place, an increase in blood will take place. This creates a gradient between the deoxygenated haemoglobin in the blood and the oxygenated haemoglobin in the blood. Because oxygen in haemoglobin is bound to the iron present, deoxygenated haemoglobin will have unbound iron ions. These respond magnetically to the magnetic field applied during the procedure.
By processing the data obtained through the procedure (which involves picking up the blood flow differences via magnetic fields and radio frequency waves), a map of brain activity emerges. Within an experiment, this is cross-referenced with a control state, whether for a patient or group of participants in a study, in order to interpret the data.
Limitations of fMRI include noise which interferes with the signals e.g. from heat in the vicinity of the scanner, movement of the participant or system noise coming from the hardware, and statistics needed to make use of the raw data. Sometimes the statistics used was not robust enough to distinguish between real differences in brain activity and noise. Famously, the fMRI data of a dead salmon was used to show real differences in brain activity obtained by using flawed statistics.
Positron emission tomography (PET) is an imaging technique that relies on a radioactively labelled molecule (a tracer) injected into the patient to pick up metabolic signals from the body. It is used in the diagnosis of cancer metastasis and Alzheimer’s disease.
The tracer used is a common molecule in the body such as glucose, water or urea, and following its injection into the patient, a waiting period is undertaken to allow for the molecule to disperse via the blood stream to the target location. After waiting for the required period of time, the patient is ready for scanning. The scanner picks up the signal given when the positron (like an electron but positive instead of negative) from the radioactively labelled glucose or other tracer is annihilated by the contact with an electron in its environment. It only travels up to 1 mm in the body before this happens.
Since the use of glucose by the brain is correlated with increase blood flow to an active area, the data can be likened to that obtained via fMRI, which also relies on the link between brain activity and blood flow.
Limitations of PET include exposure to ionising radiation from the tracer injected into the patient, a well as the procedure being expensive.
The concept of electroencephalography (EEG) is based on the ionic current produced from brain activity. This can be recorded using electrodes placed on the scalp. Unlike the other techniques, this gives a trace of different brain waves as opposed to a picture of the brain.
EEG can be used to diagnose and track the progression of epilepsy and coma. The waves are characterised by being alpha, beta, delta or theta waves based on their frequency. For example, alpha waves are of 8-12 Hz.
Limitations of EEG include low spatial resolution and a poor signal-to-noise ratio. This means that it’s very difficult to speculate which area of the brain signals might be coming from, even with using many electrodes spread out to cover all areas; and that in order to obtain good quality data for studies, a large sample of participants is required.
Effects of brain and spinal cord damage
With so many different functions to support, unsurprisingly any damage to the brain and spinal cord can have severe implications. At the brain level, information processing can be affected following injury. The difficulty in storing and retrieving information results in memory problems, commonly with short term (or working) memory.
The period of time spent in a coma affects the cognitive outcomes of patients.
Speech can also be affected. If the areas responsible for the movements required in speech are affected and cause difficulties speaking including slurred speech, it is termed dysarthria. If the coordination between voluntary movement and speech is affected, it is termed dyspraxia of speech and causes difficulty in expressing what one wants to say. This can occur in mild to severe forms.
Brain injury, and notably spinal cord injury, can both result in mobility problems as motor skills are affected. Brain injury can cause imbalance and reduced mobility. Movements may be slower, and walking may be difficult without support.
Spinal cord injury at different levels on the spine can cause a disconnection between nerves throughout the body associated with that level (height), and cause loss of sensation and movement from that point downwards. Therefore, injuries higher up the spine, such as near the neck, can cause paralysis of the whole body below that level (tetraplegia), while lower injuries can allow for retained control of the head, torso and arms (paraplegia). Tetraplegia usually involves the loss of both sensory and motor functions, while paraplegia can be sensory or motor only, as well as both.
If brain injury disturbs the pituitary gland, hormonal imbalances can occur. Since the pituitary gland secretes key hormones that regulate many functions around the body, symptoms can be very varied and include mood swings, impotence, fatigue, headaches, vision issues and others.
In case of severe injury, a state of coma can be followed by a persistent vegetative state, or brain death. A persistent vegetative state exhibits low levels of consciousness, while brain death is a lack of consciousness or ability to become conscious, inability to breathe spontaneously (apnea) and loss of reflexes. Brain death is death established via the brain.
While establishing death was trivial in the past, emerging life support technologies have made the death verdict in unresponsive patients a challenging ethical dilemma.
The ethical implications of declaring patients under various states of coma as brain dead extend to medical issues as well as legal issues. Medical issues include the continued life support given to patients in the hope that they would recover, while legal issues are concerned with the relationship between the patient’s family, their rights to determining the life support given to their relative, as well as declaring a person dead. Legally, death is a given event in time, rather than a biological process.
While the body may continue to be alive in terms of tissues and organ function (minus the brain, or at least the parts of the brain that are essential to consciousness, breathing, etc.), the personhood of the patient is irreversibly dead, as they cannot regain consciousness or stay alive without life support.
Therefore, meeting the criteria for brain death implies a death verdict, and life support is expected to end, as medically it would be futile to maintain the bodily functions of a dead person. In terms of organ transplantation, life support enables the preservation of organs for others to receive as transplants. This can be coordinated with the withdrawal of life support.
A synapse is the site of communication between the end of an axon and the beginning on a dendrite. It can also be between a neuron and a non-neuron cell such as a muscle cell. In the olden days people used to think that there were no gaps between neurons, and they just extended continuously throughout the body (silly eh?). Now we know better, much better. More for you to learn!
Let’s just get the overall picture first: a signal may be transmitted from one neurone to another via axons and dendrites. A sending neurone passes the signal to a receiving neurone which may pass it on to another receiving neurone, thus becoming itself a sending neurone…
Clearly, each nerve cell (= neurone) only has one axon but multiple dendrites. How does this regulate the way in which certain signals are deemed to pass the threshold required for them to be passed along as opposed to them ceasing there?
There are 2 ways: either multiple signals are sent via the same synapse in a short space of time, or single signals are sent via synapses at different locations. Therefore, the first is called temporal summation while the second is called spatial summation. Summation simply refers to the sum of signals sent to reach the threshold for transmission.
Another nugget to be gotten out of the way: the signal transmitted is always axon –> dendrite, unidirectional, because specific neurotransmitter receptors are only found on the dendrites!
Now let’s delve into the details…
The first is a pre-synaptic neurone, the second is a post-synaptic neurone. Before and after the synaptic gap itself, or the synaptic cleft. The action potential reaching the pre-synaptic neurone causes some calcium channels which respond to voltage to open. These are called voltage-gated ion channels. Essentially this step converts the electrical energy into chemical energy. Ca+ ions rush inside.
As a result, vesicles (membrane-bound spaces containing a specific compound) migrate towards the outer edge of the neurone membrane and fuse (exocytosis) so that their contents – neurotransmitters in our case (you know, the good stuff like serotonin, oxytocin, dopamine, etc.) – are released into the synaptic gap.
Specific neurotransmitter receptors found on the post-synaptic neurone bind the neurotransmitters causing Na+ channels to open. Na+ ions rush into the post-synaptic neurone. If they’re angry enough (we’re talking about a steep electrochemical gradient of course), an action potential will be initiated and carried forward. Chemical energy has once again been converted into electrical energy. Magic.
Not all synapses are excitatory and encourage a signal to be carried forward. Some are inhibitory and prevent an action potential being carried forward. A common signal molecule (neurotransmitter) for this is GABA. Upon binding to receptors on the membrane, it triggers an uptake of chlorine ions into the cell, or a release of sodium ions out of the cell; both of which shift the transmembrane potential downwards, making it more negative.
The effects of chemicals on nerve impulses
Many chemicals can interfere with nervous transmission in a variety of different ways. We’ll be looking at the effects of dopamine used against Parkinson’s disease, lidocaine used as an anaesthetic, and the effects of some recreational drugs such as heroin, alcohol, cannabis and methamphetamine.
Parkinson’s disease is a condition that affects the nervous system, particularly with regard to bodily movements (shaking, rigidity, slowness). It causes the brain cells that secrete the neurotransmitter dopamine to die, resulting in low dopamine levels. In the early stages of the disease, treatment with dopamine-restoring drugs can be effective.
Rotigotine is one such drug. It works by binding the dopamine receptors and restoring communication between nerves.
Lidocaine can be applied topically to the skin via a patch or cream, as well as injected. It can numb specific areas and acts as a painkiller, hence is used as an anaesthetic in surgery, dental work, etc. It works by blocking voltage-gated Na+ ion channels, hence preventing the depolarisation of the post-synaptic neurone. No pain signals can be transmitted to the brain because no signals are created in the first place.
Heroin works by acting on the same neural pathways that regulate endorphins whose role it is to offer relief from pain in situations such as exercise, stress, labour, etc. They not only relieve pain, but also produce a distinct euphoria.
By taking excess drugs that bind to the endorphin receptors, the feeling of euphoria is maintained longer and is stronger than what may come from the body’s own endorphins. Over long periods of time, however, the nerves sustain damage and the effects wear off in the presence of the same amount of drug. Persistent use turns from pleasure-seeking to mere blunting of pain caused as withdrawal symptoms arise.
Alcohol has many different effects on signal transmission in the nervous system. It acts to suppress excitatory nerve pathways while stimulating inhibitory nerve pathways (hence, it is a depressant drug). Alcohol promotes the activity of the GABA neurotransmitter which is an inhibitor, while suppressing glutamine. Overall effects from this action include slowness and sluggishness.
The effects of alcohol are stronger on the higher brain regions and function than on the lower ones. Hence, it affects the cerebral cortex and limbic system before the cerebellum, hypothalamus and pituitary gland, and medulla. As the effects progress with increasing amounts of alcohol, the symptoms of decreased inhibition, becoming more talkative, lower processing of sensory information and impaired judgement occur, followed by exaggerated emotions and memory loss.
As the effects advance to the lower parts of the brain, symptoms of impaired movement and balance, increased libido and urination occur. By the time alcohol starts to affect the medulla which governs basic, automated functions including breathing and heart rate, potentially fatal symptoms can occur, including loss of consciousness, decreased breathing and lower body temperature.
Cannabis contains the active chemical THC (Delta-9-tetrahydrocannabinol) which binds cannabinoid receptors (CB1) in the brain. These receptors are endogenously activated by the chemical anandamide which controls mood, emotion, cognition, pain, appetite, etc.
By binding these receptors, intracellular enzymes are activated which reduce the secretion of other neurotransmitters, adding to the sense of relaxation. In the reward circuits, however, the lack of these specific cannabinoid recepors results in the increase of secretion of dopamine instead. This is caused by the effect on the GABAergic neuron (as seen for alcohol) of removing the inhibition, thus allowing the secretion of dopamine.
Methamphetamine (meth) also produces its symptoms of alertness and elevated mood via dopamine release in multiple ways. Firstly, it enters the dopamine vesicles in the presynaptic neuron, causing secretion of the neurotransmitter. Secondly, it blocks the re-uptake of dopamine from the synaptic cleft into the presynaptic neuron (by blocking its transporter), resulting in a buildup of dopamine in the synaptic cleft.
This boosts signal transmission between neurons, resulting in the feelings of euphoria experienced. As for other drugs, this response can wear off if overstimulated, due to damage accrued in the dopamine axons.
Drug dependency is brought about through both physical and psychological means, resulting in symptoms of physical dependency and psychological dependency.
The biological basis of dependency underpins the physical effects. Drug abuse results in the brain resetting its baseline state higher and higher, creating a situation where increasing doses of a drug are required to elicit the same effects as before. The impact of drugs on the nervous system extends to changes in gene expression, which enable the long-term state of addiction to develop in an individual.
Attempts to go without the drug following these events will induce withdrawal. Withdrawal causes a host of physical symptoms that are severe enough to push the patient to take the drug again, rather than allow them to push through. These symptoms include shivering, nausea, diarrhoea, sweating, headaches, seizures and others. This cycle of becoming addicted, experiencing withdrawals and continuing drug use forms the basis of physical dependency.
Psychological dependency may overlap with physical dependency, since the mind is intricately connected to the physical brain, but differs in that the perception of needing to use the drug in order to function is not of a physical origin, as the withdrawals are.
Individuals may feel convinced that they require the drug in order to live their life, in order to work, in order to fall asleep, etc. If the physical addiction has been addressed, psychological addiction may well jeopardise this step by bringing the patient back into drug use.
Psychological dependency manifests through cravings. Other symptoms include anxiety when faced with quitting the drug, loss of appetite, denial, obsession with procuring and keeping the drug, insomnia and others.
Therefore, treatment and care must focus on both the physical dependency as well as the sources of the psychological dependency in order to be successful long-term.
The consequences of drug dependency stretch from the individual using drugs to their immediate environment, and further out into the wider society. Individual implications include an abandonment of other areas of life, physical and mental health damage, loss of support networks including family and friends, and compromised home, career, etc. The length of time associated with the state of dependency determines the extent to which these effects build up.
The farther implications that affect society as a whole extend to provision of healthcare, law enforcement where drug use is associated with crime, the strain suffered by family members, and public risk where high-functioning professionals such as drivers and doctors have drug dependency.