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Strychnine poisoning characteristically produces rapidly recurring, intensely painful generalized muscle spasms, precipitated by slight sensory stimuli, with consciousness initially preserved. “Strychnia” is the historical name for strychnine.

Following ingestion, manifestations commonly begin within roughly 15–60 minutes, although exposure route and amount alter the time course. Early features include apprehension, restlessness, heightened sensitivity and stiffness or twitching of the muscles, especially about the neck and back. The patient can then develop violent, generalized muscle spasms with rigid limbs and backward arching of the trunk, termed opisthotonus. Jaw closure and contraction of the facial muscles can produce trismus and risus sardonicus. The respiratory muscles may become fixed, causing difficulty breathing and cyanosis.^[ref]

Attacks may be triggered by touch, a noise, light or attempts to move the patient. During the intervals the muscles may relax substantially, and the patient may remain lucid and fearful of the next attack. Repeated contractions cause exhaustion, sweating and hyperthermia; severe cases develop acidosis, rhabdomyolysis and acute kidney injury. Death can result from respiratory failure. Consciousness can be lost late through hypoxia, so preserved awareness is a characteristic early clue, not an invariable requirement.^[ref]

This pattern helps distinguish the condition from many epileptic seizures, in which impaired awareness and a postictal state are common, and from tetanus, whose evolution is usually slower and whose rigidity tends to persist between attacks. The distinction is not absolute and symptoms alone do not prove the particular poison. A convincing forensic diagnosis combines the clinical sequence and exposure history with toxicological analysis.

The modern explanation is blockade of inhibitory glycine receptors in the spinal cord and brainstem, leaving reflex motor activity excessively excitable. This explains why trivial stimulation can cause a massive contraction. The receptor explanation is a later interpretation of the recognizable nineteenth-century syndrome.^[ref]

The assertion is too absolute: a remedy can cause a distant response through a reflex or another intervening physiological change without first being absorbed into the blood. It is substantially right for the direct action of a circulating drug on a distant target, but does not describe every remote effect of treatment.

Three mechanisms should be distinguished:

The distinction is between transport of the medicinal substance and transmission of its consequences. A reflex transmits activity in neurons; a locally acting intestinal agent changes a physical condition; a circulating drug delivers molecules to its distant target. The same remedy may combine these routes, and an apparently rapid effect does not by itself settle which route caused it.

A useful experimental design would therefore compare remote responses with measurements of the agent in blood, and would test the proposed neural pathway separately. In an appropriate physiological preparation, recording the response while interrupting a relevant afferent pathway can test whether that pathway is necessary; preserving the circulation while interrupting nerve conduction distinguishes neural transmission from vascular transport. Conversely, a remote effect after vascular transfer supports a circulating agent, provided contamination and other transferred mediators are controlled. Failure to detect a drug is only as strong as the analytical detection limit.

Absorption is one route to remote action, not a universal prerequisite for every distant physiological consequence. The historical language “animal economy” means the functioning organism; it should not conceal the distinction between a direct pharmacological effect and a secondary physiological response.

Vomiting is a coordinated nervous motor act that can be initiated from the digestive system, circulating emetic substances, the vestibular system, or higher and lower brain pathways. A cause need not lie in the stomach.

Local causes include irritant food or poisons, gastritis, gastroenteritis, gastric outlet obstruction and intestinal obstruction. Chemical irritation, inflammation or distension activates visceral sensory pathways, notably afferents of the vagus nerve, which relay to the medulla oblongata. In obstruction, retention and distension provide continuing stimulation; merely seeing food return does not imply excessive gastric contractile strength. Peritonitis and painful disease elsewhere in the abdomen can also recruit visceral afferent pathways.^[ref]

Circulating emetic agents, including some drugs and metabolic products accumulating in kidney failure, act partly through the area postrema, a chemosensitive region with unusually direct access to substances in the blood. Gastrointestinal and blood-borne inputs converge through the nucleus tractus solitarius and connected medullary networks. It is more accurate to describe interacting groups of neurons than one isolated “vomiting centre”.^[ref]

Other important groups are motion sickness, where information from the vestibular system conflicts with other sensory information; migraine and intracranial disease, including raised intracranial pressure from a brain tumour or intracranial haemorrhage; and higher-centre influences such as a repulsive sight, smell, fear or learned association. Pregnancy-associated vomiting belongs in the differential, with endocrine and central contributions rather than an explanation that it is simply mechanical pressure by the uterus upon the stomach. These causes engage different inputs to an overlapping final motor programme.^[ref]

The act itself requires several coordinated changes. The proximal stomach and lower oesophageal sphincter relax; retrograde activity can bring contents of the upper intestine into the stomach; the diaphragm and abdominal muscles generate a pressure gradient that expels the contents. During expulsion the upper passage opens while coordinated laryngeal closure helps protect the airway. Retching and actual expulsion are related stages, and neither should be confused with effortless regurgitation.^[ref]

This mechanism explains the diversity of causes: many sensory and chemical inputs can recruit the same coordinated output. A pressure recording and observation of gastrointestinal movements during an emetic response can distinguish the patterned act from a simple spontaneous return of contents; they would not, without further evidence, identify the original cause in an individual.

The glenohumeral joint combines a large humeral head with a shallow glenoid cavity. Its range of movement depends on the comparatively loose joint capsule; the glenoid labrum, rotator cuff and surrounding muscles provide stability. An injury can therefore lever the humeral head out of the glenoid cavity while tearing the joint capsule and sometimes the glenoid labrum or adjacent bone.

The historical names describe where the humeral head is found relative to the scapula and clavicle:

An 1867 answer would stress early recognition, relaxation of the muscles, and controlled traction with suitable countertraction or gentle leverage to guide the humeral head through the torn joint capsule. Anaesthesia made relaxation practicable. These are principles, not a reason to reproduce old forceful manoeuvres or indiscriminate pulley traction: force can produce a fracture or damage the axillary artery and brachial plexus.

Current assessment establishes the direction and associated fracture, usually with radiography in appropriate views. Before and after joint reduction, record pulse, perfusion, distal movement and sensation, including sensation over the lateral deltoid muscle supplied by the axillary nerve. A nerve injury accompanying joint dislocation makes prompt restoration of alignment especially important.^[ref] Joint reduction is performed by trained clinicians with suitable analgesia and, when needed, sedation or anaesthesia. Repeated forceful attempts are inappropriate; irreducibility or associated complex fracture requires specialist management.^[ref]

After joint reduction, reassess the axillary nerve and circulation and confirm alignment and relevant fractures with radiography. A temporary sling relieves pain, followed by progressive physiotherapy to restore movement and rotator cuff function. The balance is between recurrent instability and stiffness: prolonged immobilisation is not a universal solution. Recurrent instability, significant structural injury and persistent weakness require further assessment.^[ref]

The terms describe contrasting palatal architectures; their literal “old” and “new” implications do not establish which architecture was ancestral. A palaeognathous palate has extensive bracing of the palatal apparatus against the skull base, involving the vomer, pterygoid bone, palatine bone and prominent basipterygoid processes. In a neognathous palate, reduced bracing and a more mobile pterygoid–palatine connection permit greater relative movement. These are arrangements of joints and contacts, not simply differences in lower-jaw shape. The distinction concerns the structural basis of cranial kinesis, movement within the skull beyond ordinary opening of the lower jaw.^[ref]

Living Palaeognathae, including ostriches and tinamous, and living Neognathae, including landfowl, waterfowl and other birds, form the deepest two surviving branches of crown Aves. Historically, the heavily braced condition was commonly interpreted as retention of a primitive nonavian configuration, followed by evolution of a more mobile palate in Neognathae. That interpretation combined resemblance to outgroups with the misleading intuition that a lineage branching early must preserve the ancestral anatomy. A sister lineage has had just as much time to change; its living members are not ancestors of the other branch.

The difficulty is establishing character polarity when delicate palatal elements are absent, crushed or wrongly identified in fossils near the crown divergence. Comparisons of the vomer across living and extinct birds documented meaningful differences in contact geometry but also substantial variation and repeated reduction. The 2019 analysis by Han Hu and colleagues emphasized how incomplete contacts restrict inferences about extinct cranial kinesis. A single robust-looking element cannot establish an immobile skull, and one potentially mobile joint cannot establish the full range of movement. Constraints elsewhere in the kinetic chain remain relevant.^[ref]

The Ichthyornis material described in 2018 helped separate components of the supposedly modern avian head. Three-dimensionally preserved skull elements combined a small beak at the jaw tips and retained teeth with a reconstructed kinetic apparatus, while other cranial regions remained markedly dinosaurian. Thus tooth loss, beak expansion and acquisition of a mobile feeding apparatus did not form one indivisible evolutionary event. This example of mosaic evolution also weakens the argument that a toothed stem bird must have a fully rigid, palaeognath-like palate. Its importance is the combination of characters, rather than an inference that every modern kinetic mechanism was already identical.^[ref]

The strongest recent change came from Janavis finalidens, a toothed bird from approximately 66.7 million years ago, described in 2022. micro-computed tomography exposed a well-preserved pterygoid bone within the specimen. Its articular construction and comparative shape resemble those of Galloanserae, supporting a mobile pterygoid–palatine connection. The animal was recovered outside the living-bird crown group, close to Ichthyornis, rather than inside Neognathae. Consequently, anatomy previously treated as a neognath innovation occurred on an earlier branch. On that reconstruction, mobility evolved before crown Aves, and the tightly integrated palaeognathous palate is a subsequent specialization of the palaeognath lineage.^[ref]

The inference is best understood by separating observation, placement and reconstruction. The observation is the morphology of a fossil pterygoid bone. Its placement outside crown Aves comes from a wider analysis of phylogenetic characters using phylogenetics. The inference that the crown ancestor had a relatively mobile palate combines those findings with distributions of phylogenetic characters in living groups. None alone proves the entire history. Convergence in the fossil lineage remains a logical alternative; it would require a different pattern of character acquisition from ancestral mobility followed by increased bracing. Distinguishing these alternatives requires additional palatal characters and fossil sampling, not the age of the specimen alone. A 66.7-million-year-old stem bird need not predate the crown ancestor chronologically: stem and crown lineages can coexist.

Functional and developmental caution also matters. fossils generally lack ligaments, muscles and direct measurements of movement. Comparative joint geometry can support potential mobility, but cannot yield exact excursions or feeding performance without further assumptions. The palaeognathous palate should not be reduced to total skull immobility, nor every neognathous palate to one uniform kinetic mechanism. The defensible revision is that important neognath-like palatal features originated before the living-bird crown split, making palaeognath specializations a plausible derived condition. The two living clades remain valid; what changes is the inferred history of the anatomical states used to describe them.

taphonomy studies the transformation of biological remains from death or production into the material ultimately recovered and interpreted. It explains how a living organism or community becomes an incomplete geological sample. For shed structures or trace fossils, production of the evidence need not involve the death of the producer. Its relevance therefore extends beyond asking whether a skeleton was buried intact.

Three primary process classes are decay; physical disarticulation and transport; and burial alteration, including diagenetic mineralization. The boundaries are operational and the mechanisms interact: post-mortem decay can continue after burial, and previously buried remains can be reworked and transported again. biostratinomy groups events before final burial, whereas diagenesis groups subsequent physical and chemical changes. Those are stages or settings, rather than three mutually exclusive mechanisms.

First, post-mortem decay transforms tissues by autolysis, microbial decomposition and associated chemical reactions. Soft tissues, connective tissues and different phylogenetic characters disappear at different rates. The important result is not simply that hard parts survive longer: a partly decayed organism can acquire a misleading anatomical combination. Experiments on amphioxus and lamprey larvae followed recognizable characters through decomposition. Derived diagnostic features tended to disappear before some more general chordate features, producing a directional bias. Coding every unobserved diagnostic character as ancestrally absent can push a genuinely derived fossil toward an earlier position on a phylogenetic tree, the effect called stemward slippage.^[ref]

Experiments on adult hagfish and lampreys extended the comparison beyond larvae. They documented transformations as well as disappearance, so a residual stain or collapsed structure should not automatically be identified as an intact organ. Replicate specimens sampled through time are needed because destructive observations cannot follow every internal character in the same individual. For a new experimental test, temperature, water chemistry, microbial conditions and starting condition should be recorded and, where tested, varied independently. A laboratory sequence supplies constraints on interpretations; it is not a universal clock assigning an exact post-mortem duration to every fossil.^[ref]

Second, disarticulation, fragmentation and taphonomic transport alter which elements occur together and where they accumulate. Loss of ligaments releases bones, while currents or scavengers can move them. Shape, density, size, articulation and orientation influence transportability, so a concentration of robust elements need not represent the most abundant living species or the original place of death. Flow experiments and comparison of element representation, as developed in Michael R. Voorhies's vertebrate assemblage study, provide a basis for testing such alternatives. A useful comparison measures elements under specified flow and sediment conditions, with articulated versus disarticulated material distinguished. hydraulic sorting cannot be transferred unchanged between all animals and environments.^[ref]

The consequences include mixing habitats and ages. An apparently coherent bone bed may combine local and transported animals; reworking of fossils can place older remains in younger sediment; time averaging can combine successive communities into one assemblage. None implies that every fossil assemblage is hopelessly mixed. Articulation, abrasion, orientation, size distributions, sedimentary context and independent age information can instead delimit the plausible history. Abrasion alone is an imperfect transport-distance meter because material properties and the transport medium also matter.

Third, burial changes both preservation and geometry. Rapid isolation can reduce scavenging, but burial does not halt all decomposition. sedimentary compaction flattens and fractures remains; dissolution removes mineralized tissues; precipitation can infill pores or replicate tissues; fossil recrystallization can erase original microscopic detail. A fossil can therefore retain an excellent outline but lack its original chemistry, or preserve histology while its overall shape has been distorted. Mineralized replacement is not the only route to fossilization, and surviving original hard parts need not have undergone complete replacement.

Experiments by Derek E. G. Briggs and Amanda J. Kear illustrate constructive as well as destructive diagenesis. Decaying shrimps developed diagenetic mineralization by calcium phosphate preserving muscle detail, particularly in oxygen-restricted systems, with the animal itself supplying phosphate. diagenetic mineralization began on a timescale of weeks. This demonstrates a mechanism by which decay-associated chemistry can stabilize fine structures before they disappear. It does not show that low oxygen guarantees preservation: chemical availability, acidity, tissue composition and the relative rates of destruction and precipitation still control the outcome.^[ref]

These mechanisms are indispensable for reconstructing the history of life. A fossil's first occurrence is a minimum observation of a lineage, not automatically its evolutionary origin. A sudden appearance of soft-bodied organisms can reflect a new window of exceptional preservation, while disappearance of a phylogenetic character can reflect its destruction rather than evolutionary loss. Relative fossil abundance reflects both biological abundance and the probabilities of production, preservation, exposure and recovery. Comparisons of diversity through time must therefore consider changes in environments, preservational pathways and sampling. The fossil record is filtered evidence whose reliability can be tested; taphonomy identifies which biological conclusions that evidence can support.

Patch clamp connects an electrode to a small area of cell membrane through a solution-filled patch pipette. A gigaohm seal around the rim makes tiny electric currents through ion channels distinguishable from seal leak current. The beautiful change of scale is from a population's average response to individual opening and closing events in single-channel recording.

Separate two questions. The configuration determines which cell membrane is accessible: an intact patch in cell-attached recording, an excised inside-out patch or outside-out patch, or intracellular access in whole-cell recording. The recording mode determines what is commanded and what is observed: voltage clamp commands an electric potential difference and measures electric current; current clamp commands electric current and measures membrane potential. Whole-cell recording supports both modes. A patch can contain several ion channels; a small recording area does not establish that only one is present.

The 1976 article Single-channel currents recorded from membrane of denervated frog muscle fibres describes an extracellular fire-polished pipette with a $3$–$5\mu \mathrm{m}$ opening and $2$–$5\mathrm{M\Omega }$ electrical resistance. It contained saline and a channel-activating compound. Two separate intracellular electrodes supplied local voltage clamp of the muscle fibre; the patch amplifier measured local electric current. Cooling to $6$–$8{}^{\circ }\mathrm{C}$ and hyperpolarization helped resolve elementary events. Figure 2 shows step-like pulses with a $200\mathrm{Hz}$ filter at $-120\mathrm{mV}$ and $8{}^{\circ }\mathrm{C}$. Discrete amplitudes and overlapping events supported individual ion channel openings rather than a smoothly varying population response. This was neither whole-cell recording through the patch pipette nor current clamp. The specialized conditions improved visibility but limit generalization to warmer preparations; filtering can conceal brief openings.^[ref]

For a new single-channel recording experiment, useful controls include a matched recording without the activating compound, controlled membrane potential, repeated seal tests, and an explicitly stated filter frequency response. These are proposed controls, not claims that every one was performed in that 1976 figure. Changing membrane potential tests the single-channel current-voltage relation; changing the recording filter tests whether a short pulse's apparent amplitude is an instrument artifact. A flat baseline establishes neither an absence of ion channels nor an absence of very brief events.

The perineal body is a fibromuscular junction in the perineum where several muscle and connective-tissue elements meet. In female anatomy it lies between the vagina and anal canal. Its value as a support point follows from the convergence of attachments, rather than from being a separate large muscle.

Piriformis syndrome is a clinical syndrome in which pain, sometimes with numbness or radiating leg symptoms, is attributed to irritation or compression of the sciatic nerve near the piriformis muscle. The nerve and muscle lie close together in the deep buttock region, making a mechanical interaction anatomically plausible.^[ref]

Anatomical plausibility is not proof of the explanation in a particular case. A 2018 study reviewed magnetic resonance imaging and clinical records to compare people with usual and variant relationships between the sciatic nerve and piriformis muscle. It found no significant difference in the recorded frequency of piriformis syndrome, buttock pain or sciatic symptoms between the anatomical groups.^[ref] The study illustrates why an unusual scan finding must be distinguished from demonstrated symptomatic nerve compression.

Combined recording used to classify sleep and waking, commonly including electroencephalography, eye-movement signals and muscle activity. Classification of a sleep stage is not itself a measure of the content of a memory.

The popliteus is a posterior knee muscle connecting the proximal tibia with the lateral femoral region through its tendon. It contributes to controlling rotation and initiating flexion from extension. Its action depends on which skeletal segment is relatively fixed.

The popliteus tendon connects the popliteus muscle to its femoral attachment and has close relations to the lateral knee structures. Its course helps explain the muscle’s role in controlling rotation near the extended knee. Tendon continuity and joint-cavity relations are separate anatomical questions.

The posterior interosseous nerve is the continuation of the deep motor pathway of the radial nerve in the forearm. It supplies many extensor muscles. Loss of these movements can occur without the cutaneous sensory loss expected from a more proximal radial-nerve lesion.

Apparent enlargement in which increased fat or connective tissue can conceal loss of functioning muscle. Distinguish it from enlargement of working muscle fibres by hypertrophy.

The quadriceps femoris is the anterior thigh muscle group transmitting force through the quadriceps tendon, patella and patellar ligament to extend the knee. Its components do not all cross the same joints; rectus femoris also crosses the hip.

The rectoanal inhibitory reflex is relaxation of the internal anal sphincter in response to distension of the rectum. Because the internal anal sphincter is smooth muscle, this relaxation is distinct from voluntary control of the external anal sphincter. In manometry, a rectal balloon supplies a controlled distension while anal pressure sensors record the response over time.^[ref]

A fall in pressure can coexist with a contractile response elsewhere or at another time. The same study measured inhibitory and contractile reflexes and asked subjects about sensation; a relaxation trace therefore cannot simply be equated with the conscious urge to empty the rectum.^[ref]

A complementary experiment recorded tension in isolated human internal anal sphincter strips. A donor of nitric oxide relaxed the strips; blocking its synthesis suppressed relaxation evoked by electrical nerve stimulation, and arginine reversed the inhibition in a stereospecific control. These interventions support a role for nitric oxide in nerve-mediated relaxation. An isolated strip identifies a mechanism in the effector muscle; it does not reproduce the whole intact reflex circuit.^[ref]

A respiratory muscle changes the geometry or pressure of the breathing apparatus. The respiratory diaphragm enlarges the thorax during inspiration; intercostal muscles and, under suitable conditions, accessory muscles contribute. Quiet expiration can be largely passive, whereas forceful expiration recruits additional muscular activity.

Breakdown of skeletal muscle that can complicate intense generalized muscle spasms.

The rib cage is the framework formed by ribs, thoracic vertebrae, costal cartilages and the sternum. It protects thoracic organs while allowing controlled changes in volume. Joint geometry and muscle action transform this framework into a moving breathing apparatus.

A physician who distinguished external fatty growth around the heart from changes within muscle fibers. Microscopy helped separate lesions that could share a broad historical name while involving different tissue arrangements.^[ref]

Physician associated with On Fatty Diseases of the Heart by Richard Quain.

Official biography and portrait: Royal College of Physicians biography; identity and dates.

Portrait catalogue description: Portrait of Sir Richard Quain, RCP object X120.