Agnosia

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Agnosia 

Agnosia
Agnosia causes the victims to lose the ability to recognize or comprehend the meaning of objects even with intact senses.
Specialty	Psychiatry, Neurology, Neuropsychology

Picture of the ventral and dorsal streams. The ventral stream is depicted in purple and the dorsal stream is depicted in green.

 

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

Types

Name	Description
Akinetopsia	Also known as cerebral akinetopsia, this is associated with the inability to perceive visual motion. One cause of cerebral akinetopsia is lesions outside the striate cortex.
Allotopagnosia	Patients cannot point at external targets located outside their own body, whether other persons' body parts or objects, but they perfectly point at their own body parts.
Anosognosia	This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive visual agnosia	Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.[7]
Associative visual agnosia	Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Astereognosis	Also known as somatosensory agnosia, it is connected to tactile sense—that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Auditory agnosia	Auditory agnosia has been recognized since 1877. With auditory agnosia, there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal. There are two types of auditory agnosia: semantic associative and discriminative agnosia. Semantic associative agnosia is associated with lesions to the left hemisphere, whereas discriminative agnosia is associated with lesions to the right hemisphere.
Auditory verbal agnosia	Also known as pure word deafness (PWD). This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.
Autotopagnosia	Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Cerebral achromatopsia	A difficulty in perceiving colors in which the world may appear drab or in shades of gray. Cerebral achromatopsia is caused by neurological damage. There are two regions of the brain which specialize for color recognition, areas V4 and V8. If there is a unilateral lesion to area V4, a loss of color perception in only half of the visual field may result known as hemiachromatopsia. Similar, but distinct, is color agnosia, which involves having difficulty recognizing colors, while still being able to perceive them as measured by a color matching or categorizing task.
Cortical deafness	Refers to people who do not perceive any auditory information but whose hearing is intact.
Environmental agnosia	It is the inability to locate a specific room or building that one is familiar with, as well as the inability to provide directions for how to arrive at a particular location. These individuals experience difficulty with learning routes. This form of agnosia is often associated with lesions to the bilateral or right hemisphere posterior regions. It is also associated with prosopagnosia and Parkinson's disease.
Finger agnosia	Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosia	Patients perceive only parts of details, not the whole object.
Heterotopagnosia	Patients cannot point at another person's body parts, but can point at their own body parts.
Integrative agnosia	Usually a patient has a form of associative agnosia or apperceptive agnosia. However, in the case of integrative agnosia a patient falls in between a form of associative and apperceptive agnosia. This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Pain agnosia	Also referred to as congenital analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia	Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia	Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Pure alexia	Inability to recognize text. Patients with pure alexia often have damage to their corpus callosum, as well as damage to the left visual association areas. Pure alexia involves not being able to read printed material, but these individuals still have the ability to write. Individuals with pure alexia usually read words letter by letter. However, individuals with pure alexia show a frequency effect. They are able to read high frequency words better and faster than they can read low frequency words.
Semantic agnosia	Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).
Social-emotional agnosia	Sometimes referred to as expressive agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Simultagnosia	The inability to process visual input as a whole. The person instead processes faces, bodies, objects, rooms, places, pictures in a bit-by-bit fashion. When looking at a picture they can describe the parts of the picture but struggle to comprehend the picture as a whole. Simultagnosia occurs in Bálint syndrome but may also occur in brain injury. This condition can also be described by only seeing one object at a time. An example is having two cups in your visual field and only being able to see one at a time.
Tactile agnosia	Impaired ability to recognize or identify objects by touch alone.
Time agnosia	Is the loss of comprehension of the succession and duration of events.
Topographical disorientation	Also known as topographical agnosia or topographagnosia, this is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognize objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place. Patients with topographical agnosia have the ability to read maps, but become lost in familiar environments.
Visuospatial dysgnosia	This is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. It may include constructional apraxia, topographical disorientation, optic ataxia, ocular motor apraxia, dressing apraxia, and right-left confusion.
Visual agnosia	Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.

Visual agnosia

Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.

Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.

In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.

Speech agnosia

Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they do indeed hear sounds being produced, but that the sounds are fundamentally unrecognizable/untranslatable.

1. EXAMINER: What did you eat for breakfast?
2. PATIENT: Breakfast, breakfast, it sounds familiar but it doesn't speak to me. (Obler & Gjerlow 1999:45)

Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).

Causes

Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.

Patients who experience dramatic recovery from blindness experience significant to total agnosia.

The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:

• DOG activates 3, and inhibits 0 letters in DOG. – +3
• DOG activates 2, and inhibits 1 letters in FOG. – +2
• DOG activates 1, and inhibits 2 letters in DAN. – +1

The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it's understood today—speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex.

Diagnosis

In order to assess an individual for agnosia, it must be verified that the individual is not suffering from a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.

Pure alexia

Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters.

Prosopagnosia

Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture.

Treatment

For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.

Verbal strategies

Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues.

Alternate cues

Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate cues such as a scar on an individual's face or crooked teeth in order to recognize the individual. Hair color and length can be helpful cues as well.

Organizational strategies

Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues.

Alternative medicine

These strategies elicit the use of an unaffected modality. For example, visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. For example, an individual with prosopagnosia can wait for someone to speak, and will usually recognize the individual from their speech.

Current research

There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials.

History

The term 'agnosia' comes from the Ancient Greek ἀγνωσία (agnosia), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.

After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri.

Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly.

Head injury

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Head_injury 

Head injury
Soldier wounded at the Battle of Antietam on September 17, 1862.

A head injury is any injury that results in trauma to the skull or brain. The terms traumatic brain injury and head injury are often used interchangeably in the medical literature. Because head injuries cover such a broad scope of injuries, there are many causes—including accidents, falls, physical assault, or traffic accidents—that can cause head injuries.

The number of new cases is 1.7 million in the United States each year, with about 3% of these incidents leading to death. Adults have head injuries more frequently than any age group resulting from falls, motor vehicle crashes, colliding or being struck by an object, or assaults. Children, however, may experience head injuries from accidental falls or intentional causes (such as being struck or shaken) leading to hospitalization. Acquired brain injury (ABI) is a term used to differentiate brain injuries occurring after birth from injury, from a genetic disorder, or from a congenital disorder.

Unlike a broken bone where trauma to the body is obvious, head trauma can sometimes be conspicuous or inconspicuous. In the case of an open head injury, the skull is cracked and broken by an object that makes contact with the brain. This leads to bleeding. Other obvious symptoms can be neurological in nature. The person may become sleepy, behave abnormally, lose consciousness, vomit, develop a severe headache, have mismatched pupil sizes, and/or be unable to move certain parts of the body. While these symptoms happen immediately after a head injury occurs, many problems can develop later in life. Alzheimer’s disease, for example, is much more likely to develop in a person who has experienced a head injury.

Brain damage, which is the destruction or degeneration of brain cells, is a common occurrence in those who experience a head injury. Neurotoxicity is another cause of brain damage that typically refers to selective, chemically induced neuron/brain damage.

Classification

Head injuries include both injuries to the brain and those to other parts of the head, such as the scalp and skull. Head injuries can be closed or open. A closed (non-missile) head injury is where the dura mater remains intact. The skull can be fractured, but not necessarily. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater. Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area. A head injury may cause skull fracture, which may or may not be associated with injury to the brain. Some patients may have linear or depressed skull fractures. If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of intracranial hemorrhage include subdural, subarachnoid, extradural, and intraparenchymal hematoma. Craniotomy surgeries are used in these cases to lessen the pressure by draining off the blood.

Brain injury can occur at the site of impact, but can also be at the opposite side of the skull due to a contrecoup effect (the impact to the head can cause the brain to move within the skull, causing the brain to impact the interior of the skull opposite the head-impact). While impact on the brain at the same site of injury to the skull is the coup effect. If the impact causes the head to move, the injury may be worsened, because the brain may ricochet inside the skull causing additional impacts, or the brain may stay relatively still (due to inertia) but be hit by the moving skull (both are contrecoup injuries).

Specific problems after head injury can include

• Skull fracture
• Lacerations to the scalp and resulting hemorrhage of the skin
• Traumatic subdural hematoma, a bleeding below the dura mater which may develop slowly
• Traumatic extradural, or epidural hematoma, bleeding between the dura mater and the skull
• Traumatic subarachnoid hemorrhage
• Cerebral contusion, a bruise of the brain
• Concussion, a loss of function due to trauma
• Dementia pugilistica, or "punch-drunk syndrome", caused by repetitive head injuries, for example in boxing or other contact sports
• A severe injury may lead to a coma or death
• Shaken baby syndrome – a form of child abuse

Concussion

coup bruise

A concussion is a form of a mild traumatic brain injury (TBI). This injury is a result due to a blow to the head that could make the person’s physical, cognitive, and emotional behaviors irregular. Symptoms may include clumsiness, fatigue, confusion, nausea, blurry vision, headaches, and others. Mild concussions are associated with sequelae. Severity is measured using various concussion grading systems.

A slightly greater injury is associated with both anterograde and retrograde amnesia (inability to remember events before or after the injury). The amount of time that the amnesia is present correlates with the severity of the injury. In all cases, the patients develop post concussion syndrome, which includes memory problems, dizziness, tiredness, sickness and depression. Cerebral concussion is the most common head injury seen in children.

Intracranial bleeding

Types of intracranial hemorrhage are roughly grouped into intra-axial and extra-axial. The hemorrhage is considered a focal brain injury; that is, it occurs in a localized spot rather than causing diffuse damage over a wider area.

Intra-axial bleeding

Intra-axial hemorrhage is bleeding within the brain itself, or cerebral hemorrhage. This category includes intraparenchymal hemorrhage, or bleeding within the brain tissue, and intraventricular hemorrhage, bleeding within the brain's ventricles (particularly of premature infants). Intra-axial hemorrhages are more dangerous and harder to treat than extra-axial bleeds.

Extra-axial bleeding

Extra-axial hemorrhage, bleeding that occurs within the skull but outside of the brain tissue, falls into three subtypes:

• Epidural hemorrhage (extradural hemorrhage) which occur between the dura mater (the outermost meninx) and the skull, is caused by trauma. It may result from laceration of an artery, most commonly the middle meningeal artery. This is a very dangerous type of injury because the bleed is from a high-pressure system and deadly increases in intracranial pressure can result rapidly. However, it is the least common type of meningeal bleeding and is seen in 1% to 3% cases of head injury.
  • Patients have a loss of consciousness (LOC), then a lucid interval, then sudden deterioration (vomiting, restlessness, LOC)
  • Head CT shows lenticular (convex) deformity.
• Subdural hemorrhage results from tearing of the bridging veins in the subdural space between the dura and arachnoid mater.
  • Head CT shows crescent-shaped deformity
• Subarachnoid hemorrhage, which occur between the arachnoid and pia meningeal layers, like intraparenchymal hemorrhage, can result either from trauma or from ruptures of aneurysms or arteriovenous malformations. Blood is seen layering into the brain along sulci and fissures, or filling cisterns (most often the suprasellar cistern because of the presence of the vessels of the circle of Willis and their branch points within that space). The classic presentation of subarachnoid hemorrhage is the sudden onset of a severe headache (a thunderclap headache). This can be a very dangerous entity and requires emergent neurosurgical evaluation and sometimes urgent intervention.

Cerebral contusion

Cerebral contusion is bruising of the brain tissue. The piamater is not breached in contusion in contrary to lacerations. The majority of contusions occur in the frontal and temporal lobes. Complications may include cerebral edema and transtentorial herniation. The goal of treatment should be to treat the increased intracranial pressure. The prognosis is guarded.

Diffuse axonal injury

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of the damage.

Signs and symptoms

Three categories used for classifying the severity of brain injuries are mild, moderate or severe.

Mild brain injuries

Symptoms of a mild brain injury include headaches, confusion, ringing ears, fatigue, changes in sleep patterns, mood or behavior. Other symptoms include trouble with memory, concentration, attention or thinking. Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident. Narcolepsy and sleep disorders are common misdiagnoses.

Moderate/severe brain injuries

Cognitive symptoms include confusion, aggressive, abnormal behavior, slurred speech, and coma or other disorders of consciousness. Physical symptoms include headaches that do not go away or worsen, vomiting or nausea, convulsions or seizures, abnormal dilation of the eyes, inability to awaken from sleep, weakness in the extremities and loss of coordination. In cases of severe brain injuries, the likelihood of areas with permanent disability is great, including neurocognitive deficits, delusions (often, to be specific, monothematic delusions), speech or movement problems, and intellectual disability. There may also be personality changes. The most severe cases result in coma or even persistent vegetative state.

Symptoms in children

Symptoms observed in children include changes in eating habits, persistent irritability or sadness, changes in attention, disrupted sleeping habits, or loss of interest in toys.

Presentation varies according to the injury. Some patients with head trauma stabilize and other patients deteriorate. A patient may present with or without neurological deficit. Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal. Disturbance of vision and equilibrium may also occur. Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures, nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to deteriorate later.

Symptoms of skull fracture can include:

• leaking cerebrospinal fluid (a clear fluid drainage from nose, mouth or ear) is strongly indicative of basilar skull fracture and the tearing of sheaths surrounding the brain, which can lead to secondary brain infection.
• visible deformity or depression in the head or face; for example a sunken eye can indicate a maxillar fracture
• an eye that cannot move or is deviated to one side can indicate that a broken facial bone is pinching a nerve that innervates eye muscles
• wounds or bruises on the scalp or face.
• Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.

Because brain injuries can be life-threatening, even people with apparently slight injuries, with no noticeable signs or complaints, require close observation; They have a chance for severe symptoms later on. The caretakers of those patients with mild trauma who are released from the hospital are frequently advised to rouse the patient several times during the next 12 to 24 hours to assess for worsening symptoms.

The Glasgow Coma Scale (GCS) is a tool for measuring the degree of unconsciousness and is thus a useful tool for determining the severity of the injury. The Pediatric Glasgow Coma Scale is used in young children. The widely used PECARN Pediatric Head Injury/Trauma Algorithm helps physicians weigh risk-benefit of imaging in a clinical setting given multiple factors about the patient—including mechanism/location of the injury, age of the patient, and GCS score.

Location of brain damage predicts symptoms

Symptoms of brain injuries can also be influenced by the location of the injury and as a result, impairments are specific to the part of the brain affected. Lesion size is correlated with severity, recovery, and comprehension. Brain injuries often create impairment or disability that can vary greatly in severity.

Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomia, unknowingly making up words (neologisms), and problems with comprehension. The symptoms of Wernicke’s aphasia are caused by damage to the posterior section of the superior temporal gyrus.

Damage to the Broca’s area typically produces symptoms like omitting functional words (agrammatism), sound production changes, dyslexia, dysgraphia, and problems with comprehension and production. Broca’s aphasia is indicative of damage to the posterior inferior frontal gyrus of the brain.

An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired, however. For example, in pure alexia, the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca's area and Wernicke's area). However, this does not mean one suffering from pure alexia is incapable of comprehending speech—merely that there is no connection between their working visual cortex and language areas—as is demonstrated by the fact that pure alexics can still write, speak, and even transcribe letters without understanding their meaning.

Lesions to the fusiform gyrus often result in prosopagnosia, the inability to distinguish faces and other complex objects from each other. Lesions in the amygdala would eliminate the enhanced activation seen in occipital and fusiform visual areas in response to fear with the area intact. Amygdala lesions change the functional pattern of activation to emotional stimuli in regions that are distant from the amygdala.

Other lesions to the visual cortex have different effects depending on the location of the damage. Lesions to V1, for example, can cause blindsight in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure. Lesions to V4 can cause color-blindness, and bilateral lesions to MT/V5 can cause the loss of the ability to perceive motion. Lesions to the parietal lobes may result in agnosia, an inability to recognize complex objects, smells, or shapes, or amorphosynthesis, a loss of perception on the opposite side of the body.

Causes

Head injuries can be caused by a large variety of reasons. All of these causes can be put into two categories used to classify head injuries; those that occur from impact (blows) and those that occur from shaking. Common causes of head injury due to impact are motor vehicle traffic collisions, home and occupational accidents, falls, assault, and sports related accidents. Head injuries from shaking are most common amongst infants and children.

According to the United States CDC, 32% of traumatic brain injuries (another, more specific, term for head injuries) are caused by falls, 10% by assaults, 16.5% by being struck by or against something, 17% by motor vehicle accidents, and 21% by other/unknown ways. In addition, the highest rate of injury is among children ages 0–14 and adults age 65 and older. Brain injuries that include brain damage can also be brought on by exposure to toxic chemicals, lack of oxygen, tumors, infections, and stroke. Possible causes of widespread brain damage include birth hypoxia, prolonged hypoxia (shortage of oxygen), poisoning by teratogens (including alcohol), infection, and neurological illness. Brain tumors can increase intracranial pressure, causing brain damage.

Diagnosis

There are a few methods used to diagnose a head injury. A healthcare professional will ask the patient questions revolving around the injury as well as questions to help determine in what ways the injury is affecting function. In addition to this hearing, vision, balance, and reflexes may also be assessed as an indicator of the severity of the injury. A non-contrast CT of the head should be performed immediately in all those who have suffered a moderate or severe head injury. A CT is an imaging technique that allows physicians to see inside the head without surgery in order to determine if there is internal bleeding or swelling in the brain. Computed tomography (CT) has become the diagnostic modality of choice for head trauma due to its accuracy, reliability, safety, and wide availability. The changes in microcirculation, impaired auto-regulation, cerebral edema, and axonal injury start as soon as a head injury occurs and manifest as clinical, biochemical, and radiological changes. An MRI may also be conducted to determine if someone has abnormal growths or tumors in the brain or to determine if the patient has had a stroke.

Glasgow Coma Scale (GCS) is the most widely used scoring system used to assess the level of severity of a brain injury. This method is based on objective observations of specific traits to determine the severity of a brain injury. It is based on three traits eye-opening, verbal response, and motor response, gauged as described below. Based on the Glasgow Coma Scale severity is classified as follows, severe brain injuries score 3–8, moderate brain injuries score 9-12 and mild score 13–15.

There are several imaging techniques that can aid in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS), positron emission tomography (PET), single-photon emission tomography (SPECT). CT scans and MRI are the two techniques widely used and are the most effective. CT scans can show brain bleeds, fractures of the skull, fluid build up in the brain that will lead to increased cranial pressure. MRI is able to better detect smaller injuries, detect damage within the brain, diffuse axonal injury, injuries to the brainstem, posterior fossa, and subtemporal and sub frontal regions. However, patients with pacemakers, metallic implants, or other metal within their bodies are unable to have an MRI done. Typically the other imaging techniques are not used in a clinical setting because of the cost, lack of availability.

Management

Most head injuries are of a benign nature and require no treatment beyond analgesics such as acetaminophen. Non-steroidal painkillers such as ibuprofen are avoided since they could make any potential bleeding worse. Due to the high risk of even minor brain injuries, close monitoring for potential complications such as intracranial bleeding. If the brain has been severely damaged by trauma, a neurosurgical evaluation may be useful. Treatments may involve controlling elevated intracranial pressure. This can include sedation, paralytics, cerebrospinal fluid diversion. Second-line alternatives include decompressive craniectomy (Jagannathan et al. found a net 65% favorable outcomes rate in pediatric patients), barbiturate coma, hypertonic saline, and hypothermia. Although all of these methods have potential benefits, there has been no randomized study that has shown unequivocal benefit.

Clinicians will often consult clinical decision support rules such as the Canadian CT Head Rule or the New Orleans/Charity Head injury/Trauma Rule to decide if the patient needs further imaging studies or observation only. Rules like these are usually studied in depth by multiple research groups with large patient cohorts to ensure accuracy given the risk of adverse events in this area.

There is a subspecialty certification available for brain injury medicine that signifies expertise in the treatment of brain injury.

Prognosis

Prognosis, or the likely progress of a disorder, depends on the nature, location, and cause of the brain damage (see Traumatic brain injury, Focal and diffuse brain injury, Primary and secondary brain injury). 

In children with uncomplicated minor head injuries the risk of intracranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post-traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a longboard. If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one-sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily exposes patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

Brain injuries are very hard to predict in the outcome. Many tests and specialists are needed to determine the likelihood of the prognosis. People with minor brain damage can have debilitating side effects; not just severe brain damage has debilitating effects. The side- effects of a brain injury depend on location and the body’s response to injury. Even a mild concussion can have long term effects that may not resolve.

History

The foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case studies by Paul Broca. The first case study on Phineas Gage’s head injury is one of the most astonishing brain injuries in history. In 1848, Phineas Gage was paving way for a new railroad line when he encountered an accidental explosion of a tamping iron straight through his frontal lobe. Gage observed to be intellectually unaffected but exemplified post-injury behavioral deficits. These deficits include: becoming sporadic, disrespectful, extremely profane, and gave no regard for other workers. Gage started having seizures in February 1860, dying only four months later on May 21, 1860.

Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca’s first patient lacked productive speech. He saw this as an opportunity to address language localization. It wasn't until Leborgne, formally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left cerebral hemisphere. The affected areas are known today as Broca’s area and Broca’s Aphasia.

A few years later, a German neuroscientist, Carl Wernicke, consulted on a stroke patient. The patient experienced neither speech nor hearing impairments but suffered from a few brain deficits. These deficits included: lacking the ability to comprehend what was spoken to him and the words written down. After his death, Wernicke examined his autopsy that found a lesion located in the left temporal region. This area became known as Wernicke's area. Wernicke later hypothesized the relationship between Wernicke's area and Broca's area, which was proven fact.

Epidemiology

Head injury is the leading cause of death in many countries.

Ötzi

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/%C3%96tzi 

Ötzi
Pronunciation	German pronunciation: [ˈœtsi] (listen)
Born	c. 3345 BCE near the present village of Feldthurns (Velturno), north of Bolzano, Italy
Died	c. 3300 BCE (aged about 45) Ötztal Alps, near Hauslabjoch on the border between Austria and Italy
Other names	Ötzi the Iceman Similaun Man Man from Hauslabjoch Hauslabjoch mummy Frozen Man Frozen Fritz Tyrolean Iceman Similaun Man (Italian: Mummia del Similaun)
Known for	Oldest natural mummy of a Chalcolithic (Copper Age) European man
Height	1.6 m (5 ft 3 in)
Website	South Tyrol Museum of Archaeology

Ötzi, also called the Iceman, is the natural mummy of a man who lived between 3400 and 3100 BCE. The mummy was found in September 1991 in the Ötztal Alps, hence the nickname "Ötzi", near Similaun mountain and Hauslabjoch on the border between Austria and Italy.

Ötzi is believed to have been murdered; an arrowhead has been found in his left shoulder, which would have caused a fatal wound. The circumstances of his death and those of his life are the subject of much investigation and speculation.

He is Europe's oldest known natural human mummy and has offered an unprecedented view of Chalcolithic (Copper Age) Europeans. His body and belongings are displayed in the South Tyrol Museum of Archaeology in Bolzano, South Tyrol, Italy.

Discovery

Discovery site marked on a map of the Alps

 

Ötzi was found on 19 September 1991 by two German tourists, at an elevation of 3,210 metres (10,530 ft) on the east ridge of the Fineilspitze in the Ötztal Alps on the Austrian–Italian border. The tourists, Helmut and Erika Simon, were walking off the path between the mountain passes Hauslabjoch and Tisenjoch. They believed that the body was of a recently deceased mountaineer. The next day, a mountain gendarme and the keeper of the nearby Similaunhütte first attempted to remove the body, which was frozen in ice below the torso, using a pneumatic drill and ice-axes, but had to give up due to bad weather. The next day, eight groups visited the site, among whom were mountaineers Hans Kammerlander and Reinhold Messner. The body was semi-officially extracted on 22 September and officially salvaged the following day. It was transported to the office of the medical examiner in Innsbruck, together with other objects found. On 24 September, the find was examined there by archaeologist Konrad Spindler of the University of Innsbruck. He dated the find to be "about four thousand years old", based on the typology of an axe among the retrieved objects.

Border dispute

At the Treaty of Saint-Germain-en-Laye of 1919, the border between North and South Tyrol was defined as the watershed of the rivers Inn and Etsch. Near Tisenjoch the glacier (which has since retreated) complicated establishing the watershed and the border was drawn too far north. Although Ötzi's find site drains to the Austrian side, surveys in October 1991 showed that the body had been located 92.56 m (101.22 yd) inside Italian territory as delineated in 1919 (Coordinates: 46°46′45.8″N 10°50′25.1″E.) The province of South Tyrol claimed property rights but agreed to let Innsbruck University finish its scientific examinations. Since 1998, it has been on display at the South Tyrol Museum of Archaeology in Bolzano, the capital of South Tyrol.

Scientific analyses

The corpse has been extensively examined, measured, X-rayed, and dated. Tissues and intestinal contents have been examined microscopically, as have the items found with the body. In August 2004, frozen bodies of three Austro-Hungarian soldiers killed during the Battle of San Matteo (1918) were found on the mountain Punta San Matteo in Trentino. One body was sent to a museum in the hope that research on how the environment affected its preservation would help unravel Ötzi's past.

Body

Ötzi the Iceman while still frozen in the glacier, photographed by Helmut Simon upon the discovery of the body in September 1991

 

By current estimates (2016), at the time of his death, Ötzi was 160 centimetres (5 ft 3 in) tall, weighed about 50 kilograms (110 lb), and was about 45 years of age. When his body was found, it weighed 13.750 kilograms (30 lb 5.0 oz). Because the body was covered in ice shortly after his death, it had only partially deteriorated. Initial reports claimed that his penis and most of his scrotum were missing, but this was later shown to be unfounded. Analysis of pollen, dust grains and the isotopic composition of his tooth enamel indicates that he spent his childhood near the present village of Feldthurns, north of Bolzano, but later went to live in valleys about 50 kilometres farther north.

In 2009, a CAT scan revealed that the stomach had shifted upward to where his lower lung area would normally be. Analysis of the contents revealed the partly digested remains of ibex meat, confirmed by DNA analysis, suggesting he had a meal less than two hours before his death. Wheat grains were also found. It is believed that Ötzi most likely had a few slices of a dried, fatty meat, probably bacon, which came from a wild goat in South Tyrol, Italy. Analysis of Ötzi's intestinal contents showed two meals (the last one consumed about eight hours before his death), one of chamois meat, the other of red deer and herb bread; both were eaten with roots and fruits. The grain also eaten with both meals was a highly processed einkorn wheat bran, quite possibly eaten in the form of bread. In the proximity of the body, and thus possibly originating from the Iceman's provisions, chaff and grains of einkorn and barley, and seeds of flax and poppy were discovered, as well as kernels of sloes (small plum-like fruits of the blackthorn tree) and various seeds of berries growing in the wild.

Hair analysis was used to examine his diet from several months before. Pollen in the first meal showed that it had been consumed in a mid-altitude conifer forest, and other pollens indicated the presence of wheat and legumes, which may have been domesticated crops. Pollen grains of hop-hornbeam were also discovered. The pollen was very well preserved, with the cells inside remaining intact, indicating that it had been fresh (estimated about two hours old) at the time of Ötzi's death, which places the event in the spring or early summer. Einkorn wheat is harvested in the late summer, and sloes in the autumn; these must have been stored from the previous year.

High levels of both copper particles and arsenic were found in Ötzi's hair. This, along with Ötzi's copper axe blade, which is 99.7% pure copper, has led scientists to speculate that Ötzi was involved in copper smelting.

By examining the proportions of Ötzi's tibia, femur and pelvis, Christopher Ruff has determined that Ötzi's lifestyle included long walks over hilly terrain. This degree of mobility is not characteristic of other Copper Age Europeans. Ruff proposes that this may indicate that Ötzi was a high-altitude shepherd.

Using modern 3D scanning technology, a facial reconstruction has been created for the South Tyrol Museum of Archaeology in Bolzano, Italy. It shows Ötzi looking old for his 45 years, with deep-set brown eyes, a beard, a furrowed face, and sunken cheeks. He is depicted looking tired and ungroomed.

Health

Ötzi apparently had whipworm (Trichuris trichiura), an intestinal parasite. During CT scans, it was observed that three or four of his right ribs had been cracked when he had been lying face down after death, or where the ice had crushed his body. One of his fingernails (of the two found) shows three Beau's lines indicating he was sick three times in the six months before he died. The last incident, two months before he died, lasted about two weeks. It was also found that his epidermis, the outer skin layer, was missing, a natural process from his mummification in ice. Ötzi's teeth showed considerable internal deterioration from cavities. These oral pathologies may have been brought about by his grain-heavy, high carbohydrate diet. DNA analysis in February 2012 revealed that Ötzi was lactose intolerant, supporting the theory that lactose intolerance was still common at that time, despite the increasing spread of agriculture and dairying.

Skeletal details and tattooing

Ötzi had a total of 61 tattoos, consisting of 19 groups of black lines ranging from 1 to 3 mm in thickness and 7 to 40 mm long. These include groups of parallel lines running along the longitudinal axis of his body and to both sides of the lumbar spine, as well as a cruciform mark behind the right knee and on the right ankle, and parallel lines around the left wrist. The greatest concentration of markings is found on his legs, which together exhibit 12 groups of lines. A microscopic examination of samples collected from these tattoos revealed that they were created from pigment manufactured out of fireplace ash or soot.

Radiological examination of Ötzi's bones showed "age-conditioned or strain-induced degeneration" corresponding to many tattooed areas, including osteochondrosis and slight spondylosis in the lumbar spine and wear-and-tear degeneration in the knee and especially in the ankle joints. It has been speculated that these tattoos may have been related to pain relief treatments similar to acupressure or acupuncture. If so, this is at least 2,000 years before their previously known earliest use in China (c. 1000 BCE). Recent research into archaeological evidence for ancient tattooing has confirmed that Ötzi is the oldest tattooed human mummy yet discovered.

Clothes and shoes

Archeoparc (Schnals valley / South Tyrol). Museum: Reconstruction of the neolithic clothes worn by Ötzi

 

Ötzi wore a cloak made of woven grass and a coat, a belt, a pair of leggings, a loincloth and shoes, all made of leather of different skins. He also wore a bearskin cap with a leather chin strap. The shoes were waterproof and wide, seemingly designed for walking across the snow; they were constructed using bearskin for the soles, deer hide for the top panels, and a netting made of tree bark. Soft grass went around the foot and in the shoe and functioned like modern socks. The coat, belt, leggings and loincloth were constructed of vertical strips of leather sewn together with sinew. His belt had a pouch sewn to it that contained a cache of useful items: a scraper, drill, flint flake, bone awl and a dried fungus.

An artist's impression of Ötzi's right shoe

The shoes have since been reproduced by a Czech academic, who said that "because the shoes are actually quite complex, I'm convinced that even 5,300 years ago, people had the equivalent of a cobbler who made shoes for other people". The reproductions were found to constitute such excellent footwear that it was reported that a Czech company offered to purchase the rights to sell them. However, a more recent hypothesis by British archaeologist Jacqui Wood says that Ötzi's shoes were actually the upper part of snowshoes. According to this theory, the item currently interpreted as part of a backpack is actually the wood frame and netting of one snowshoe and animal hide to cover the face.

The leather loincloth and hide coat were made from sheepskin. Genetic analysis showed that the sheep species was nearer to modern domestic European sheep than to wild sheep; the items were made from the skins of at least four animals. Part of the coat was made from domesticated goat belonging to a mitochondrial haplogroup (a common female ancestor) that inhabits central Europe today. The coat was made from several animals from two different species and was stitched together with hides available at the time. The leggings were made from domesticated goat leather. A similar set of 6,500-year-old leggings discovered in Switzerland were made from goat leather which may indicate the goat leather was specifically chosen.

Shoelaces were made from the European genetic population of cattle. The quiver was made from wild roe deer, the fur hat was made from a genetic lineage of brown bear which lives in the region today. Writing in the journal Scientific Reports, researchers from Ireland and Italy reported their analysis of his clothing's mitochondrial DNA, which was extracted from nine fragments from six of his garments, including his loin cloth and fur cap.

Tools and equipment

Ötzi lithic assemblage
a) Dagger, b) Endscraper, c) Borer, d) Arrowhead 14, e) Arrowhead 12, f) Small flake 

 

Other items found with the Iceman were a copper axe with a yew handle, a chert-bladed knife with an ash handle and a quiver of 14 arrows with viburnum and dogwood shafts. Two of the arrows, which were broken, were tipped with flint and had fletching (stabilizing fins), while the other 12 were unfinished and untipped. The arrows were found in a quiver with what is presumed to be a bow string, an unidentified tool, and an antler tool which might have been used for sharpening arrow points. There was also an unfinished yew longbow that was 1.82 metres (72 in) long.

A replica of Ötzi's copper axe

In addition, among Ötzi's possessions were berries, two birch bark baskets, and two species of polypore mushrooms with leather strings through them. One of these, the birch fungus, is known to have anthelmintic properties, and was probably used for medicinal purposes. The other was a type of tinder fungus, included with part of what appeared to be a complex firelighting kit. The kit featured pieces of over a dozen different plants, in addition to flint and pyrite for creating sparks.

Ötzi's copper axe was of particular interest. His axe's haft is 60 centimetres (24 in) long and made from carefully worked yew with a right-angled crook at the shoulder, leading to the blade. The 9.5 centimetres (3.7 in) long axe head is made of almost pure copper, produced by a combination of casting, cold forging, polishing, and sharpening. Despite the fact that copper ore sources in the Alpines are known to have been exploited at the time, a study indicated that the copper in the axe came from southern Tuscany. It was let into the forked end of the crook and fixed there using birch-tar and tight leather lashing. The blade part of the head extends out of the lashing and shows clear signs of having been used to chop and cut. At the time, such an axe would have been a valuable possession, important both as a tool and as a status symbol for the bearer.

Genetic analysis

Ötzi's full genome has been sequenced; the report on this was published on 28 February 2012. The Y chromosome DNA of Ötzi belongs to a subclade of G defined by the SNPs M201, P287, P15, L223 and L91 (G-L91, ISOGG G2a2b, former "G2a4"). He was not typed for any of the subclades downstreaming from G-L91; however, an analysis of his BAM file revealed that he belongs to the L166 and FGC5672 subclades below L91. G-L91 is now mostly found in South Corsica.

Analysis of his mitochondrial DNA showed that Ötzi belongs to the K1 subclade, but cannot be categorized into any of the three modern branches of that subclade (K1a, K1b or K1c). The new subclade has provisionally been named K1ö for Ötzi. A multiplex assay study was able to confirm that the Iceman's mtDNA belongs to a previously unknown European mtDNA clade with a very limited distribution among modern data sets.

By autosomal DNA, Ötzi is most closely related to southern Europeans, especially to geographically isolated populations like Corsicans and Sardinians.

DNA analysis also showed him at high risk of atherosclerosis and lactose intolerance, with the presence of the DNA sequence of Borrelia burgdorferi, possibly making him the earliest known human with Lyme disease. A later analysis suggested the sequence may have been a different Borrelia species.

A 2012 paper by paleoanthropologist John Hawks suggests that Ötzi had a higher degree of Neanderthal ancestry than modern Europeans.

In October 2013, it was reported that 19 modern Tyrolean men were descendants of Ötzi or of a close relative of Ötzi. Scientists from the Institute of Legal Medicine at Innsbruck Medical University had analysed the DNA of over 3,700 Tyrolean male blood donors and found 19 who shared a particular genetic mutation with the 5,300-year-old man.

Blood

In May 2012, scientists announced the discovery that Ötzi still had intact blood cells. These are the oldest complete human blood cells ever identified. In most bodies this old, the blood cells are either shrunken or mere remnants, but Ötzi's have the same dimensions as living red blood cells and resembled a modern-day sample.

H. pylori analysis

In 2016, researchers reported on a study from the extraction of twelve samples from the gastrointestinal tract of Ötzi to analyze the origins of the Helicobacter pylori in his gut. The H. pylori strain found in his gastrointestinal tract was, surprisingly, the hpAsia2 strain, a strain today found primarily in South Asian and Central Asian populations, with extremely rare occurrences in modern European populations. The strain found in Ötzi's gut is most similar to three modern individuals from Northern India; the strain itself is, of course, older than the modern Northern Indian strain.

Cause of death

The Ötzi memorial near Tisenjoch. Ötzi was found ca. 70 m NE of here, a place indicated with a red mark (not in this photo). The mountain in the background is the Fineilspitze.

 

Naturalistic reconstruction of Ötzi – South Tyrol Museum of Archaeology

The cause of death remained uncertain until 10 years after the discovery of the body. It was initially believed that Ötzi died from exposure during a winter storm. Later it was speculated that Ötzi might have been a victim of a ritual sacrifice, perhaps for being a chieftain. This explanation was inspired by theories previously advanced for the first millennium BCE bodies recovered from peat bogs such as the Tollund Man and the Lindow Man.

Arrowhead and blood analyses

In 2001, X-rays and a CT scan revealed that Ötzi had an arrowhead lodged in his left shoulder when he died and a matching small tear on his coat. The discovery of the arrowhead prompted researchers to theorize Ötzi died of blood loss from the wound, which would probably have been fatal even if modern medical techniques had been available. Further research found that the arrow's shaft had been removed before death, and close examination of the body found bruises and cuts to the hands, wrists and chest and cerebral trauma indicative of a blow to the head. One of the cuts was to the base of his thumb that reached down to the bone but had no time to heal before his death. Currently, it is believed that Ötzi bled to death after the arrow shattered the scapula and damaged nerves and blood vessels before lodging near the lung.

Recent DNA analyses claim they revealed traces of blood from at least four other people on his gear: one from his knife, two from a single arrowhead, and a fourth from his coat. Interpretations of these findings were that Ötzi killed two people with the same arrow and was able to retrieve it on both occasions, and the blood on his coat was from a wounded comrade he may have carried over his back. Ötzi's posture in death (frozen body, face down, left arm bent across the chest) could support a theory that before death occurred and rigor mortis set in, the Iceman was turned onto his stomach in the effort to remove the arrow shaft.

Alternate theory of death

In 2010, it was proposed that Ötzi died at a much lower altitude and was buried higher in the mountains, as posited by archaeologist Alessandro Vanzetti of the Sapienza University of Rome and his colleagues. According to their study of the items found near Ötzi and their locations, it is possible that the iceman may have been placed above what has been interpreted as a stone burial mound but was subsequently moved with each thaw cycle that created a flowing watery mix driven by gravity before being re-frozen. While archaeobotanist Klaus Oeggl of the University of Innsbruck agrees that the natural process described probably caused the body to move from the ridge that includes the stone formation, he pointed out that the paper provided no compelling evidence to demonstrate that the scattered stones constituted a burial platform. Moreover, biological anthropologist Albert Zink argues that the iceman's bones display no dislocations that would have resulted from a downhill slide and that the intact blood clots in his arrow wound would show damage if the body had been moved up the mountain. In either case, the burial theory does not contradict the possibility of a violent cause of death.

Legal dispute

Italian law entitled the Simons to a finders' fee from the South Tyrolean provincial government of 25% of the value of Ötzi. In 1994 the authorities offered a "symbolic" reward of 10 million lire (€5,200), which the Simons declined. In 2003, the Simons filed a lawsuit which asked a court in Bolzano to recognize their role in Ötzi's discovery and declare them his "official discoverers". The court decided in the Simons' favor in November 2003, and at the end of December that year the Simons announced that they were seeking US$300,000 as their fee. The provincial government decided to appeal.

In addition, two people came forward to claim that they were part of the same mountaineering party that came across Ötzi and discovered the body first:

• Magdalena Mohar Jarc, a retired Slovenian climber, who alleged that she discovered the corpse first after falling into a crevice, and shortly after returning to a mountain hut, asked Helmut Simon to take photographs of Ötzi. She cited Reinhold Messner, who was also present in the mountain hut, as the witness to this.
• Sandra Nemeth, from Switzerland, who contended that she found the corpse before Helmut and Erika Simon, and that she spat on Ötzi to make sure that her DNA would be found on the body later. She asked for a DNA test on the remains, but experts believed that there was little chance of finding any trace.

In 2005 the rival claims were heard by a Bolzano court. The legal case angered Mrs. Simon, who alleged that neither woman was present on the mountain that day. In 2005, Mrs. Simon's lawyer said: "Mrs. Simon is very upset by all this and by the fact that these two new claimants have decided to appear 14 years after Ötzi was found." In 2008, however, Jarc stated for a Slovene newspaper that she wrote twice to the Bolzano court in regard to her claim but received no reply whatsoever.

In 2004, Helmut Simon died. Two years later, in June 2006, an appeals court affirmed that the Simons had indeed discovered the Iceman and were therefore entitled to a finder's fee. It also ruled that the provincial government had to pay the Simons' legal costs. After this ruling, Mrs. Erika Simon reduced her claim to €150,000. The provincial government's response was that the expenses it had incurred to establish a museum and the costs of preserving the Iceman should be considered in determining the finder's fee. It insisted it would pay no more than €50,000. In September 2006, the authorities appealed the case to Italy's highest court, the Court of Cassation.

On 29 September 2008 it was announced that the provincial government and Mrs. Simon had reached a settlement of the dispute, under which she would receive €150,000 in recognition of Ötzi's discovery by her and her late husband and the tourist income that it attracts.

"Ötzi's curse"

Influenced by the "Curse of the pharaohs" and the media theme of cursed mummies, claims have been made that Ötzi is cursed. The allegation revolves around the deaths of several people connected to the discovery, recovery and subsequent examination of Ötzi. It is alleged that they have died under mysterious circumstances. These people include co-discoverer Helmut Simon and Konrad Spindler, the first examiner of the mummy in Austria in 1991. To date, the deaths of seven people, of which four were accidental, have been attributed to the alleged curse. In reality hundreds of people were involved in the recovery of Ötzi and are still involved in studying the body and the artifacts found with it. The fact that a small percentage of them have died over the years has not been shown to be statistically significant.